C Iani

University of Rome Tor Vergata, Roma, Latium, Italy

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Publications (23)52.41 Total impact

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    ABSTRACT: Recent research has shown that following stroke patients can display ipsilateral activity reflecting a functional link between the undamaged hemisphere and the affected upper limb on the same side of the body. In the present study the capacity for ipsilateral activation is documented during recovery by using transcranial magnetic stimulation (TMS) and transcranial Doppler (TCD). Fourteen patients affected by hemispheric stroke were examined with TMS and TCD within 48 h of onset, and again 6 months later. Neurological signs were scored with reference to the NIHSS, and patients executed a thumb to finger opposition task so as to further estimate the motor deficit. Twenty healthy volunteers represented the control population. (1) Both TMS and TCD yielded homogeneous results showing ipsilateral activity between affected hands and undamaged hemispheres. On stimulating the motor cortex 3 cm anterior and 3 cm lateral to Cz, a scalp site remote from the primary motor area, ipsilateral motor evoked potentials (iMEPs) from hand muscles were found in recovered patients. (2) In 8 controls iMEPs with smaller amplitudes than patients could be obtained by stimulating only the left hemisphere. (3) TCD revealed increased blood flow velocity in the ipsilateral MCA by activating the recovering hand (10.5+/-3.3%; P<0.001). TMS reveals a specific area in the motor cortex from which ipsilateral MEPs can be elicited and both TMS and TCD indicate that an ipsilateral corticospinal tract can be accessible in some adult controls or becomes unmasked after cerebral damage.
    Clinical Neurophysiology 11/2000; 111(11):1990-6. · 3.14 Impact Factor
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    ABSTRACT: To reverse the profile of abnormal intracortical excitability in patients with ALS by administering drugs that promote GABAergic transmission. Transcranial magnetic stimulation (TMS) has revealed abnormalities of cortical inhibition in ALS, a reduction of the silent period, and the absence of intracortical inhibition normally occurring in response to paired TMS. Impaired inhibitory transmission could play a role in the physiopathology of this illness. Using paired TMS with conditioning stimuli from 1-to-6-msec-interstimulus intervals, we investigated 16 patients with ALS. The protocol included: (1) the "drug-free" profile of paired TMS; (2) paired TMS 30 minutes after the intake of diazepam (3.5 mg); (3) paired TMS after 3 weeks' treatment with gabapentin (GBP) (600 mg/day) or riluzole (50 mg/twice a day). Intracortical inhibition is lost in patients with ALS, and this abnormal profile is reversed by diazepam or sustained treatment with GBP. We also noted that motor-evoked potential amplitudes to single stimuli increased (p<0.01) after diazepam and GBP. The demonstration of pharmacologic reversal of hyperexcitability in patients with ALS makes a potentially significant contribution toward understanding the pathophysiology of a disease that has so far eluded an effective cure.
    Neurology 02/2000; 54(1):58-64. · 8.30 Impact Factor
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    ABSTRACT: In the present study, the effects of benzodiazepines (diazepam) were evaluated in terms of cortical excitability changes, as tested with transcranial magnetic simulation (TMS). In particular, analyzed were drug-induced changes regarding two selected parameters of TMS: (1) the cortical excitability threshold and (2) the silent period duration (SP). For this purpose, we evaluated the effects of long-term therapy with diazepam in the patients affected by anxiety disorders and the changes induced by single oral doses of diazepam in both healthy controls and patients. In addition, we tested cortical excitability changes in two 'extreme conditions' where a considerable concentration of serum benzodiazepine-like activity was reached, as represented by diazepam overdose and idiopathic recurrent stupor (IRS). In both groups of patients, a significant increment of motor threshold was found, while in the overdose patients, the SP was also increased. The administration of flumazenil in these two conditions was followed by a prompt reversal effect, consisting of a return to normal cortical excitability parameters. The long-term usage of diazepam in patients with anxiety disorders is associated with significantly increased threshold; the increased value of these parameters was temporarily further enhanced by the administration of a single oral dose of diazepam, which, in normal control subjects, is not associated with changes of cortical excitability. The results of this study reveal that different physio-pathological conditions induced by the influence of benzodiazepine and its antagonist are reflected in excitability changes which attest to the involvement and modification of cortical GABAergic activity.
    Brain Research 02/1999; 815(2):192-9. · 2.88 Impact Factor
  • Transplantation Proceedings 01/1999; 31(1-2):404-5. · 0.95 Impact Factor
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    ABSTRACT: We report the case of a young man from the south of India, initially presenting the typical signs of benign monomelic amyotrophy (BMA) in the left upper limb. After several years, the involvement of other limbs and the appearance of bulbar signs suggested the possible diagnosis of the Madras pattern of motor neuron disease (MMND). Serial motor evoked potential (MEP) recordings allowed detection of the onset of a focal involvement of upper motor neurons (UMN) controlling innervation in the originally amyotrophic limb. Therefore, serial MEP recordings can be useful for the early detection of sub-clinical UMN damage in motor neuron disease presenting with pure lower motor neuron (LMN) signs.
    Electroencephalography and Clinical Neurophysiology 01/1999; 109(6):523-6.
  • American Journal of Hematology 12/1998; 51(2):179 - 180. · 4.00 Impact Factor
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    ABSTRACT: The aim of this study is to provide neurophysiologic evidence of ipsilateral hemispheric activation in patients affected by intracerebral gliomas via the use of transcranial magnetic stimulation. The mechanisms involved in such ipsilateral activation have yet to be established, but they may involve preexisting routes that either are suppressed or undetected in the normal brain. Ipsilateral pathways may act in reserve, activated by the impairment of contralateral control. This hypothesis is suggested by the fact that the considerable size of the tumors in our patients is not matched by a proportionate loss of motor performance in the limbs contralateral to the affected hemisphere. However, it remains possible that ipsilateral motor-evoked potentials (iMEPs) may reflect reorganizational changes without significant functional effects. The effects of such activation were investigated using both focal and nonfocal coils stimulating cortical motor areas, with MEPs recorded from both left and right thenar muscles. Fifteen healthy control subjects and seven patients were examined. iMEPs were generally absent in normal subjects, but in contrast they were obtained in the patients by stimulating the healthy hemisphere using both round and figure-of-eight coils. Distinct from contralateral MEPs, iMEPs are obtained with higher thresholds (range, 60 to 80% of stimulator output) and display longer latencies (20.9 msec versus 19.4 msec). Taken in conjunction with recent research using functional imaging brain exploration and a variety of clinical, anatomic, and neurophysiologic studies, our results reflect a growing awareness of ipsilateral motor control and its potential compensatory role when contralateral routes are damaged.
    Neurology 08/1998; 51(1):196-202. · 8.30 Impact Factor
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    ABSTRACT: In this study we introduce a new combination treatment of plasma exchange (PE) and high daily doses of prednisone for severe forms of myasthenia gravis (MG). The clinical efficacy of the combined therapy has been tested in 18 patients suffering from severe forms of MG. The protocol included 5 sessions of PE, performed in a range of 15 days, 1 session every 3 days, with concurrent administration of oral prednisone (1 mg/kg of body weight), starting at the first session of PE and given daily for at least 3 months. At the end of the entire cycle of PE, almost complete recovery (more than 90% of the initial clinical score) was obtained in 8 of 18 patients while an improvement between 60 and 90% of the initial score was achieved in 9 of 18 patients. An early improvement was noted 24 h after the beginning of plasmapheresis in 11 of 18 patients. No recurrence of symptoms was reported after 36 months of follow-up for 17 patients. The administration of steroid therapy was never followed by an early exacerbation of myasthenic symptoms as reported when it is administered in the absence of concomitant PE. According to our results, we can conclude that high doses of oral prednisone therapy in simultaneous association with PE lead to successful control of severe forms of MG, significantly superior to the therapeutic strategies until now adopted and reported in literature.
    Artificial Organs 03/1998; 22(2):129-34. · 1.96 Impact Factor
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    ABSTRACT: In this study we introduced and tested the clinical efficacy of a combined treatment based on the association of plasma exchange (PE) with high daily doses of prednisone in 18 patients with severe forms of myasthenia gravis (MG). A myasthenic score based on strength and resistance was evaluated in each patient in basal condition and during the treatment. The study design included 5 sessions of PE, performed within a period of 15 days, 1 session every 3 days, associated with administration of oral prednisone (1 mg/kg of body weight), which began at the same time as the first session and was continued following a daily schedule for at least three months. A significant improvement was obtained from the start of the therapy, with a reduction of the myasthenic score from 26.56 to 11.44 by day 10 and with further reduction after PE interruption. An early improvement, recorded within 24-48 hours of the beginning of the study design, was observed in 11/18. The administration of steroid therapy was never followed by a worsening of myasthenic symptoms (as reported when it is administered in the absence of concomitant PE). No recurrence of symptoms was reported after 29 months' follow-up. This type of therapeutic association was generally well tolerated and no unwanted side effects were observed. According to our results we can conclude that medium-high doses of oral prednisone in simultaneous association with PE lead to a successful control of severe forms of MG and may be considered a valid therapeutic strategy.
    Functional neurology 01/1998; 13(3):231-7. · 1.86 Impact Factor
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    Journal of Neurology Neurosurgery & Psychiatry 09/1997; 63(2):259-60. · 4.92 Impact Factor
  • RIVISTA ITALIANA DI PEDIATRIA. 01/1997; 23:448-453.
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    ABSTRACT: The present study aims to provide neurophysiological evidence of ipsilateral activation during motor recovery in patients after stroke. The effects of cortical reorganization were investigated using magnetic brain stimulation in order to record motor evoked potentials (MEPs) both from contralateral and ipsilateral hands. Ten healthy subjects and 13 patients were examined. The patients had suffered their first hemispheric stroke and consequent motor deficit. While ipsilateral responses (iMEPs) were absent in normal subjects, they were obtained from both ipsilateral and contralateral hands in patients. The ipsilateral MEP differed from contralateral MEP in the following respects: (1) elicitation during contraction; (2) a shorter latency; (3) a lower amplitude. The presence of optimal iMEPs (lower excitability threshold, larger amplitude) in recovered hands points to a role for the undamaged hemisphere, and in particular to the involvement of secondary motor areas. We suggest that iMEPs in general may be a marker of brain plasticity, and that the specific type described here appear in the context of fast autochthonous motor recovery.
    Neuroreport 08/1996; 7(11):1756-60. · 1.40 Impact Factor
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    ABSTRACT: We studied a 51-year-old man with multiple system atrophy and autonomic insufficiency. He had repeated episodes of loss of contact, staring, and masticatory automatisms. Blood pressure during these events documented a systolic pressure of 60 mm Hg. Cardiovascular reflex tests provided evidence of autonomic failure. Head computed tomography (CT) revealed moderate, diffuse cortical and cerebellar atrophy. These events were strictly related to blood pressure decreases and could be reproduced consistently by having the patient sit up after a meal. Ictal polygraphic recordings showed EEG changes consistent with anoxia, preceded by sudden hypotension with fixed heart rate. Cerebral anoxia during a syncopal attack may therefore precipitate transient, sudden neurologic dysfunction that closely mimics complex partial seizures. Masticatory automatisms may represent a release phenomenon resulting from inactivation of neocortical structures by cerebral anoxia or reticular disconnection.
    Epilepsia 08/1996; 37(7):690-3. · 3.91 Impact Factor
  • American Journal of Hematology 03/1996; 51(2):179-80. · 4.00 Impact Factor
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    ABSTRACT: In this study, we have used paired transcranial stimulation of the motor cortex to test the hypothesis that cortical inhibition is decreased in juvenile myoclonic epilepsy (JME). The double shock technique was adopted here because it offers a means for highlighting abnormal inhibitory mechanisms. From previous experiments performed on healthy subjects, it is known that a magnetic conditioning stimulus, of subthreshold intensity, suppresses the MEP in response to a subsequent suprathreshold stimulus delivered after 1-4 msec. JME patients were selected as a potential contrast with other forms of idiopathic generalized epilepsy, because they complain of myoclonic jerks without loss of consciousness, indicating with certainty a dysfunction of the motor cortex. Two patients with sporadic grand mal and one non-epileptic patient were also investigated. Paired stimulation was produced by a Bi-stim (Magstim) stimulator, with a figure-of-8 coil placed over the hand area of the motor cortex, and a set of interstimulus intervals (ISIs) ranging from 1 to 6 msec was analyzed. In JME patients there were two indications of abnormality with respect to normal subjects and to the other epileptic patients: (1) the absence of MEP suppression to paired stimulation; (2) a progressive amplitude increase of MEPs to the test stimulus alone. In the two patients with the other form of epilepsy the pattern of inhibition was broadly preserved, even though there was some difference from the normal profile. The results suggest that the loss of MEP inhibition can be regarded as a marker of JME.
    Electroencephalography and Clinical Neurophysiology 02/1996; 98(1):14-9.
  • Engineering Fracture Mechanics 01/1996; 53(6). · 1.41 Impact Factor
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    ABSTRACT: Aim of the study was to analyze the characteristics of motor action potentials recruitment during magnetic trans-cranial stimulation (TCS) of the brain. Coaxial needle recordings from hand and upper limb musculature, as well as surface electrodes were employed in 20 healthy controls during magnetic TCS with regular and figure-of-8 coil in different experimental protocols including: (a) simple reaction time paradigm during which TCS at subthreshold intensity for eliciting MEPs in relaxation was delivered at various intervals between the signal to move and the onset of the voluntary EMG burst; (b) suprathreshold TCS was randomly delivered while the subject was voluntarily firing at a regular rate one 'low' and/or 'high threshold' motor unit action potential (MUAP). The pre- and post-TCS MUAPs recruitment as well as their firing rates were compared; (c) recordings with two separate needles picking up individual MUAPs from the same or from two different muscles were obtained in order to test 'synchrony' of MUAP's discharge before and after TCS; (d) the influence of the time-interval separating the last discharged MUAP from TCS was evaluated. (e) differences between simultaneous surface and depth recordings were examined. The following results were obtained. (a) The same low-amplitude MUAP which is first voluntarily recruited at the onset of the EMG burst is the one initially fired by TCS in the pre-movement period. Latency shortenings and amplitude enlargement of surface MEPs were observed with faster reaction times. Such changes were coupled to the recruitment of high-threshold MUAPs being larger in amplitude and briefer in latency than the initial one. (b) When using suprathreshold TCS, MEPs followed by silent periods were found. The SP was followed by a rebound acceleration of the MUAPs firing rate compared with pre-TCS levels. Besides rebound acceleration, new MUAPs of larger amplitude than the original (= pre-stimulus) ones were recruited beyond the voluntary control. This phenomenon-together with longer SPs- was progressively more pronounced with stronger stimuli. (c) TCS was affecting the 'synchrony' of MUAPs. (d) If the latency difference between the last pre-stimulus spike and the TCS was exceeding the half-cycle of the MUAP 'natural' firing, the SP was longer in duration. (e) SPs not preceded by MEPs were clearly present in depth recordings. Surface recordings mainly reflected the behavior of high-threshold and large MUAPs.
    Brain Research 05/1995; 676(2):314-24. · 2.88 Impact Factor
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    ABSTRACT: In the context of a study of the effects of gamma-vinyl-GABA (GVG) on seizure occurrence and on EEG abnormalities we present three cases with focal epilepsy in which new clinical and EEG paroxysmal manifestations were observed during GVG therapy. At that time, whereas an amelioration or no change in patients' habitual seizures were observed, myoclonic jerks appeared with related changes in the EEG paroxysmal abnormalities, represented by generalized polyspike and wave complexes. An electroclinical correlation was recorded in one case. These data indicate that, although occurring rarely, it is possible to have epileptic myoclonus during GVG treatment. Mechanisms underlying these manifestations are difficult to explain. Probably a shift in the anti/proconvulsant GABAergic balance towards the latter may compromise the therapeutic effect of GVG.
    Acta Neurologica Scandinavica 02/1995; 91(1):1-5. · 2.47 Impact Factor
  • Electroencephalography and Clinical Neurophysiology 01/1995; 95(3).
  • Electroencephalography and Clinical Neurophysiology 01/1995; 95(3).