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Biomedical subjects

Vittorio Di Piero

Publications and source records attributed to Vittorio Di Piero.

7 recordsLinked to original sources

Clinical, cognitive, and neurophysiologic correlates of short-term treatment with carbamazepine, oxcarbazepine, and levetiracetam in healthy volunteers.

BACKGROUND: The adverse effects of the antiepileptic drugs (AEDs) originally developed are well known, while those of the newer AEDs remain unclear. OBJECTIVE: To investigate clinical, cognitive, and neurophysiologic effects of carbamazepine, oxcarbazepine, and levetiracetam in healthy volunteers. METHODS: A double-blind crossover study was conducted in 10 volunteers. Eight-day treatment with carbamazepine, oxcarbazepine, levetiracetam, or placebo was administered in random order. Drug doses were titrated gradually to the daily target doses on day 7: carbamazepine 800 mg, oxcarbazepine 1200 mg, and levetiracetam 1500 mg. At baseline and at the end of each treatment period, participants underwent cognitive and neurophysiologic assessment. A washout period of 14 days between treatment periods was conducted. RESULTS: More adverse events were self-reported with carbamazepine (63%) than the other treatments (oxcarbazepine 12%, levetiracetam 20%, placebo 5%; p < 0.001 between the 4 groups). Carbamazepine induced the greatest motor slowing (p = 0.002), followed by oxcarbazepine (p = 0.01). Levetiracetam left baseline motor speed unchanged. All AEDs increased attention span from baseline values as shown on the Stroop test. Quantitative electroencephalogram (EEG) analysis showed that carbamazepine significantly increased the delta-theta power and reduced the frequency of alpha rhythm; oxcarbazepine induced smaller changes than carbamazepine. Levetiracetam did not change any EEG measurements. On color visually evoked potential (VEP) tests, carbamazepine induced a constant slowing of P1 latency, while oxcarbazepine induced changes only after the blue-black pattern. All color VEP measures for volunteers receiving levetiracetam were almost unchanged. CONCLUSIONS: After short-term treatment in healthy volunteers, carbamazepine induced major clinical and neurophysiologic changes. Oxcarbazepine was better tolerated than carbamazepine. Levetiracetam interfered least with clinical and neurophysiologic test results.

Adult↗

A cerebral blood flow study on tonic pain activation in man.

This study examined brain areas involved in tonic pain perception. Cerebral blood flow was assessed by dynamic Xenon-133 inhalation single-photon emission tomography (SPET) in 7 healthy right-handed male volunteers undergoing the cold pressor test (CPT). In single experimental sessions, each subject was scanned twice, once in the resting state and once while immersing the left hand in freezing water (0 degrees C +/- 1). Immersion of the hand induced severe pain (visual analogue scale: 6.9 +/- 1.9) in all subjects. After correction for pCO2, cerebral blood flow was analyzed by placing a template of square regions of interest (ROIs) over 5 selected tomographic slices. Relative to the resting-state values, during the CPT, flow determinations revealed a 7-8% regional blood flow increase in the contralateral frontal lobe and bilateral temporal regions and a 15% flow increase in a ROI located over the primary sensorimotor cortex in the tomogram at 80 mm above the orbito-meatal line (corresponding to the cortical somatotopic representation of the hand) contralateral to the stimulated side. The tonic pain induced by the CPT thus appears to activate the contralateral frontal and bilateral temporal regions and more prominently, the primary sensorimotor cortex. This pattern of activation suggests that tonic painful stimuli activate the cortex partly via complex circuits and partly via direct somatosensory pathways.

Adult↗

Stroke beyond the first hours: the role of monitoring.

It is now recognized that a specialized multidisciplinary team, focusing on the care of stroke patients, leads to lower mortality and better outcomes. The positive effect of stroke units in regard to the outcome of stroke patients seems to be related to the careful monitoring of clinical parameters and clinical emergencies. The monitoring of physiological parameters in the acute phase of stroke can be considered an important management tool that can improve significantly the quality of care provided. It allows timely detection and correction of complications and consequently has a beneficial effect on outcome.

Acute Disease↗

Functional neuroimaging in acute stroke.

To the present day, the first and most widespread diagnostic approach in the assessment of acute stroke remains CT scan. Its sensitivity is very high (nearly 100%) in detecting intracerebral hemorrhage in the acute period, but its capability of revealing ischemic injury in the very first hours from symptom onset is relatively poor. Since the efficacy of thrombolytic treatment in acute stroke has been suggested by the ECASS and NINDS rt-PA trials, functional neuroimaging able to distinguish potentially salvageable tissue from irreversibly injured areas has acquired primary importance. The possibility to correctly identify the tissue of the ischemic penumbra within the first hours from symptom onset is essential for correct patient selection for thrombolitic treatment. Different imaging strategies are available for the definition of perfusion deficits within the acute time window; among these are positron emission tomography (PET), single photon emission computed tomography (SPECT), Xenon CT (XeCT), dynamic CT perfusion imaging (CTP), diffusion weighted magnetic resonance imaging (DW-MRI), and perfusion weighted magnetic resonance imaging (PW-MRI). Though each technique has its advantages and limitations to present day functional MRI remains the most widespread imaging technique in the assessment of acute stroke being more accessible than both SPECT and PET, and capable of giving information on both perfusion and tissue functional status in a single imaging session. In this paper we discuss the role of functional neuroimaging in acute stroke.

Brain Ischemia↗