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Biomedical subjects

C N Gandolfo

Publications and source records attributed to C N Gandolfo.

6 recordsLinked to original sources
PubMed1995

Motor activation time in Parkinson's disease.

Motor activation time (MAT), considered in the present work as the actual intracerebral processing delay during a reaction time (RT) task, was assessed in 17 patients with Parkinson's disease (PD) and in 7 age-matched healthy volunteers. MAT was calculated by subtracting from the premotor RT the afferent and efferent times obtained by sensory and motor evoked potentials. When compared with healthy volunteers, patients exhibited significantly (p < 0.02) prolonged MATs. In a smaller group of 9 PD patients MAT and the auditory P3 event related potential were assessed while on antiparkinsonian treatment and after a 12-hour withdrawal period. During the off medication condition patients showed a significant slowing (p < 0.01) of MAT values without any remarkable change in P3 latency or amplitude. These results suggest that MAT slowing indicates an abnormal function of the dopaminergic mechanism involved in the initiation of movement which is not related to changes in the arousal or cognitive state.

Electromyography↗
PubMed1994

Multiple sclerosis: assessment of lesional levels by means of transcranial stimulation.

Conduction in the Pyramidal Tracts (PTs) was studied in 30 healthy volunteers and 17 patients with definite Multiple Sclerosis. Central motor conduction time (CMCT) was assessed employing unipolar electrical transcranial stimulation and studies of the peripheral conduction time. Fourteen out of the seventeen studied patients showed CMCT abnormalities. No significative correlation was found between the intensity of muscle weakness and the slowness of conduction in the corresponding PTs. Subclinical abnormalities were detected in more than half of the studied patients. CMCT slowness showed a good correlation with the time course of the disease in the cortico-cervical (CCT) but not in the cortico-lumbar (CLT) tracts. Evidence favoring the existence of two different lesional levels along the PSs was found in 9 out of the 14 patients studied with recordings in the hand and leg muscles. Two patterns of abnormalities gave support to this conclusion. The first consisted of slowed conduction or inexcitability in both the CCT and CLT at one side, while only one of the contralateral PTs was impaired. In the second one, the 4 explored PTs showed a slowed conduction, but in addition, CMCT difference between the CLT and CCT was longer than normal. Both patterns suggest that one lesional level could be situated between the internal capsula and the lower cervical cord and the other in the spine below the 8th cervical methamera or in the corona radiata.

Adolescent↗
PubMed1992

Electrophysiological assessment of spinal cord lesions by means of transcranial cortical stimulation.

Central Motor Conduction Time (CMCT) was assessed in 30 healthy volunteers and 22 patients with spinal cord lesions due to compressive, degenerative and demyelinating disease. To obtain the CMCT, electrical Transcranial Stimulation and Percutaneous Spinal Stimulation or F wave calculations were employed. Pyramidal Tract (PT) conduction was always abnormal in the clinically impaired corticospinal tracts of all the studied patients. This results correlated with the degree of muscle weakness specially in those having compressive lesions. Subclinical evidence of pyramidal damage was also observed in two patients with Multiple Sclerosis. As opposed to the other groups, patients with degenerative spinal disease, showed essentially symmetric abnormalities. An important overlap of CMCT slowness was seen among the three studied groups, suggesting that this isolated clue is not valuable enough for aetiological suspicion. Double muscle responses due to single TCS were obtained, during rest, in some patients from each group, but never in controls. This pathological feature, not reported by others, could represent the excitation of indirect corticospinal connections, partially responsible for the residual motor function after PT damage.

Adolescent↗
PubMed1991

Percutaneous cervical stimulation: effects on intraspinal structures.

Changes in the amplitude of motor evoked potentials (MEPs) from percutaneous cervical stimulation (PCS) obtained at rest in the thenar muscles, and smaller than 0.8 mV, were studied under 3 different experimental conditions. A significant enhancement was observed mainly with a conditioning subthreshold transcranial stimulus and when MEPs were obtained in coincidence with weak voluntary contraction of the target muscle. Subthreshold stimulation of Ia fibers of the median nerve seemed to have a smaller facilitatory effect. It is generally accepted that PCS excites the spinal motoneuron (SMN) axons at the spinal nerve. However, our results show that other SMNs, usually not recruited, may be triggered by PCS when they receive excitatory postsynaptic potentials from the pyramidal tract (PT) or Ia fibers. This behavior suggests that low intensity PCS also exerts subthreshold excitation of the PT fibers and, perhaps, of the incoming spindle afferents, which adds its effects to the conditioning stimuli.

Adolescent↗
PubMed1990

Central motor conduction in ischaemic and hemorrhagic cerebral lesions.

Electrical Transcranial Cortical Stimulation was performed in 20 healthy volunteers and 14 patients having supra- or infratentorial vascular lesions. Central Conduction Time (CCT) in the Pyramidal Tract (PT) was calculated by subtraction of the Peripheral Conduction Time and the spinal synaptic delay to the Motor Evoked Potential (MEP) latency. Twelve out of fourteen patients showed prolonged MEP latencies or CCTs in the affected corporal segments. Only in 3 cases, 2 with subcortical hematoma and other with bilateral ischaemic lesions, the PT was inexcitable. Two patients, one with a discrete cortical lesion and the other with an hemispheric cerebellar infarct showed no abnormalities in pyramidal conduction. Electrophysiological results showed a good correspondence with the degree of clinical impairment.

Adult↗