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Biomedical subjects

U Sabatini

Publications and source records attributed to U Sabatini.

At least 19 recordsLinked to original sources
PubMed1998

Normal frontal perfusion in patients with frozen gait.

We have studied the frontal perfusion in the resting condition of two groups of patients with frozen gait: 10 patients with the syndrome of "isolated gait ignition failure" (IGIF) and 8 patients with idiopathic Parkinson's disease (PD) and severe "off" freezing. These patients were compared with two other groups: one including 20 age-matched volunteers as normal control subjects and the other one including 12 patients with progressive supranuclear palsy (PSP) as a positive control with expected frontal hypoperfusion. Frontal perfusion was assessed using single photon emission computed tomography (SPECT) regional cerebral blood flow measurement with intravenous 133Xenon. A significant frontal hypoperfusion was only present in the PSP group but not in the three others. These results do not support the hypothesis that start hesitations and freezing when walking are related to a frontal lobe dysfunction. However, it is possible that frontal neuronal dysfunction occurs without measurable cerebral blood flow changes in the resting condition.

Aged↗
PubMed1998

Cortical motor overactivation in parkinsonian patients with L-dopa-induced peak-dose dyskinesia.

We have studied the regional cerebral blood flow (rCBF) changes induced by the execution of a finger-to-thumb opposition motor task in the supplementary and primary motor cortex of two groups of parkinsonian patients on L-dopa medication, the first one without L-dopa induced dyskinesia (n = 23) and the other with moderate peak-dose dyskinesia (n = 15), and of a group of 14 normal subjects. Single photon emission tomography with i.v. 133Xe was used to measure the rCBF changes. The dyskinetic parkinsonian patients exhibited a pattern of response which was markedly different from those of the normal subjects and non-dyskinetic parkinsonian patients, with a significant overactivation in the supplementary motor area and the ipsi- and contralateral primary motor areas. These results are compatible with the hypothesis that an hyperkinetic abnormal involuntary movement, like L-dopa-induced peak dose dyskinesia, is due to a disinhibition of the primary and associated motor cortex secondary to an excessive outflow of the pallidothalamocortical motor loop.

Aged↗
PubMed1997

The ipsilateral cerebellar hemisphere is overactive during hand movements in akinetic parkinsonian patients.

We compared the rCBF changes induced by the execution of a finger-to-thumb opposition motor task in the cerebellar hemispheres of 12 normal subjects, 12 parkinsonian patients whose medication had been withheld for at least 18 h and 16 parkinsonian patients on medication using single photon emission tomography and i.v. 133Xe. The normal subjects and parkinsonian patients on medication exhibited the same pattern of response, with a significant increase in rCBF in the contralateral primary motor cortex and in the supplementary motor areas. No significant rCBF change was detected in the cerebellum of these two groups; this finding was expected since our technique cannot detect cerebellar activation when the motor task is executed at a relatively low rate and small amplitude as it was in this study. The parkinsonian patients off medication exhibited a markedly different pattern of activation characterized by a significant overactivation in the ipsilateral cerebellar hemisphere and a significant underactivation in the supplementary motor areas. These results suggest that parkinsonian patients off medication may try to compensate for their basal ganglia-cortical loop's dysfunction using other motor pathways involving cerebellar relays.

Brain Mapping↗
PubMed1996

Involvement of the limbic system in multiple sclerosis patients with depressive disorders.

This study investigates the relationship between depression and both anatomic and cerebral blood flow abnormalities in multiple sclerosis (MS) patients. Ten nondepressed MS patients were compared with 10 depressed MS patients matched for age, sex, and functional disability. Both groups were evaluated by means of neuropsychological tests, magnetic resonance imaging, and single-photon emission tomography imaging. There was no difference between the two groups with regard to the global cognitive score. Magnetic resonance imaging data showed no significant differences in the number, side, location, and area of the demyelinating lesions between the two groups; however, regional cerebral blood flow asymmetries in the limbic cortex did distinguish the two groups. Analysis of variance showed a significant effect of depression on the perfusion asymmetries in the limbic cortex. Finally, perfusion asymmetries in limbic cortex significantly correlated with depression test scores. Our findings suggest that depression in MS patients could be induced by a disconnection between subcortical and cortical areas involved in the function of the limbic system.

Adult↗
PubMed1996

Motor recovery after stroke. Morphological and functional brain alterations.

The aim of this study was to evaluate the relationships of morphological and CBF patterns with both the severity and the evolution of the motor deficit in the late phase of stroke and, in particular, to identify morphological and/or functional brain alterations associated with a persistent severe motor deficit or a poor, delayed motor recovery. We analysed CT/MRI and single photon emission tomography (SPET) findings from 37 patients studied in the chronic phase of stroke (mean duration +/- SD = 3.6 +/- 1.6 months), whom we were able to follow clinically for a period of 3 months. The eventual degree of motor recovery correlated significantly (negatively) with the time since stroke at entry, but not with the severity of neurological impairment at entry. The volume, side and location (cortical or subcortical) of the infarct did not correlate with either the severity or the evolution of the motor deficit. Patients with a CT/MRI lesion of the parietal lobe (n = 8) showed a more severe motor deficit than those with other cortical locations. The severity of the motor deficit correlated significantly (negatively) with CBF values in the supplementary motor area (SMA) and parietal areas of the damaged hemisphere, and in the contralateral undamaged primary motor cortex. The degree of motor improvement correlated significantly (positively) with CBF values in the contralateral undamaged thalamus, lentiform and caudate nuclei, and premotor cortex. In the late phase of stroke, the severity of the motor deficit may be positively associated with the functional impairment of associative parietal and frontal areas of the damaged hemisphere. The functional impairment of the basal ganglia-frontal network in the undamaged hemisphere seems to be related to a poor, delayed motor recovery.

Aged↗
PubMed1995

Presurgical integrated MRI/SPECT localization of the sensorimotor cortex in a patient with a low-grade astrocytoma in the rolandic area.

We describe the case of a young man who, despite the presence of a tumour in the left sensorimotor cortex, exhibited no motor deficit. Integrated MRI/SPECT-CBF study during motor activation was aimed at determining which cerebral areas were involved in movement execution in this patient and their relationship with the tumour. CBF changes during motor activation were located in two motor areas: anteriorly and medially to the tumour in the left frontal lobe (+29%) and in the right medial frontal cortex (+43%). Integrated MRI/SPECT images provided both an anatomical and functional definition of the motor areas in a patient with a rolandic tumour and could prove useful in determining preoperatively an appropriate surgical strategy.

Adolescent↗
PubMed1995

Abnormal vestibuloocular reflex cancellation in multiple system atrophy and progressive supranuclear palsy but not in Parkinson's disease.

We have measured the gain of the vestibuloocular reflex (VOR) in darkness and its cancellation by fixation in 37 patients with Parkinson's disease (PD), 26 patients with multiple system atrophy (MSA), 11 patients with progressive supranuclear palsy (PSP), and 19 normal volunteers. The capacity to cancel the VOR by fixation (VOR cancellation) was significantly reduced in the MSA and PSP patients compared with the PD and normal subjects (p < 10(-4)). A VOR cancellation < 90% (i.e., the mean VOR cancellation of the normals--2 SD) was present in four PD patients, 23 MSA patients, and 11 PSP patients. This criteria distinguished PD and MSA with a 89% sensitivity and a 89% specificity. Our results demonstrate that the VOR cancellation is impaired in most patients with MSA and PSP but not with PD. In MSA patients, the abnormal VOR cancellation is probably not related to the nigrostriatal dopaminergic deficit and more likely reflects a cerebellar dysfunction. Impaired VOR cancellation is a clinical criteria to differentiate MSA and PSP from PD.

Age Factors↗
PubMed1995

Prolonged muscular flaccidity after stroke. Morphological and functional brain alterations.

Patients with a motor deficit due to ischaemic stroke usually develop muscular spasticity, but in some cases they may remain with a prolonged muscular flaccidity which impairs their recovery. Little is known about the causes of these two different functional outcomes. We correlated CT/MRI and 99mTc HM-PAO SPECT with clinical findings in 42 patients at a mean time interval of 3 months after stroke. The patients were divided into two cohorts with either flaccid (prolonged muscular flaccidity) or spastic (muscular spasticity) hemiparesis. Although patients with prolonged muscular flaccidity had a greater motor deficit, the mean structural volume of the ischaemic lesion was similar to that of the muscular spasticity cohort. There was a significantly higher prevalence of structural involvement of the lentiform nucleus in prolonged muscular flaccidity cases. Relative perfusion in the lentiform nucleus, thalamus and contralateral cerebellar hemisphere was significantly lower in prolonged muscular flaccidity than in muscular spasticity patients. A subgroup with only subcortical structural lesions also showed significantly lower relative perfusion in the ipsilateral frontal association areas. A primary involvement of the lentiform nucleus by the structural lesion seems to be crucial for the persistence of flaccidity after stroke. However, cerebral blood flow (CBF) changes in other structurally intact regions indicate their additional role. It is likely that both subcortical-cortical loops involved in motor control, i.e. cortex-basal ganglia-thalamus-cortex and cortex-pons-cerebellum-thalamus-cortex, are more widely and more severely affected in patients with prolonged muscular flaccidity.

Adult↗
PubMed1994

Naltrexone, an opiate antagonist, fails to modify motor symptoms in patients with Parkinson's disease.

One month of adjunct treatment with naltrexone (100 mg/day) was compared with placebo in a double-blind, randomized, cross-over design in two groups of patients with Parkinson's disease. The first group was composed of 10 patients with a moderate motor impairment insufficiently controlled by monotherapy with bromocriptine. The second group was composed of eight patients with L-dopa-induced peak-dose dyskinesia. Naltrexone as compared with placebo did not demonstrate any significant change in motor function in either group. These negative clinical results do not support a significant role of endogenous opioid systems in the pathophysiology of motor impairment in Parkinson's disease.

Aged↗
PubMed1994

Normal activation of the supplementary motor area in patients with Parkinson's disease undergoing long-term treatment with levodopa.

Regional cerebral blood flow (rCBF) changes in cortical motor areas were measured during a movement of the dominant right hand in 15 patients with Parkinson's disease deprived of their usual levodopa treatment, in 11 patients with Parkinson's disease undergoing long-term treatment with levodopa, and in 15 normal volunteers. The supplementary motor areas were significantly activated in the normal subjects and in the patients receiving levodopa but not in the patients deprived of levodopa. The contralateral primary sensory motor area was significantly activated in all three groups. The ipsilateral primary sensory motor cortex was not activated in the normal subjects and the non-treated patients but was in the patients treated with levodopa. It is concluded that the supplementary motor area hypoactivation which is observed in akinetic non-treated patients with Parkinson's disease is not present in patients undergoing long-term treatment with levodopa. This result suggests that (a) levodopa improves the functional activity of supplementary motor areas in Parkinson's disease and (b) there is no pharmacological tolerance to this effect. The ipsilateral primary motor cortex activation observed in the patients treated with levodopa could be related to levodopa-induced abnormal involuntary movements.

Adult↗
PubMed1994

Motor recovery after early brain damage. A case of brain plasticity.

BACKGROUND: Motor recovery is remarkable when the brain is damaged early in life. We describe a case of early damage to the right hemisphere with remarkable reorganization and plastic functional changes, studied by computed neuroimaging. CASE DESCRIPTION: A 31-year-old man had a left-sided hemiplegia at the age of 12, followed by good motor recovery despite a large right cortical-subcortical lesion. Single-photon emission computed tomography with motor activation study showed cerebral blood flow increase in the left premotor and sensorimotor cortices irrespective of the hand he was moving, without flow changes in the right hemisphere. CONCLUSIONS: A remarkable reorganization and plastic brain functional changes occurred in a patient after early diffuse damage of the right hemisphere. The study points to a potential role of ipsilateral cortical efferent pathways in subserving hand movements after early cerebral damage.

Adult↗
PubMed1993

Effect of side and rate of stimulation on cerebral blood flow changes in motor areas during finger movements in humans.

We measured, using single photon emission computed tomography, the regional CBF (rCBF) changes in the motor areas of 24 right-handed normal volunteers during the performance of a motor task consisting of sequential finger-to-thumb opposition. Twelve of them performed the task with their right and their left hands consecutively with a fast frequency and large amplitude. The other 12 subjects performed the task with their right hand only at a slow frequency and small amplitude. The contralateral primary sensorimotor areas (S1/M1), supplementary motor area (SMA), and ipsilateral cerebellum were significantly activated during right and left finger movements performed at fast frequency and large amplitude. No significant difference was found between the rCBF changes induced by the right dominant and left nondominant hands. When the task was performed with a slow rate and small amplitude, the SMA was significantly activated while no significant changes were observed in the contralateral S1/M1 or in the ipsilateral cerebellum. These results demonstrate (a) that hand dominance evokes no differences in the activation of the main motor areas and (b) that the frequency and amplitude of the movement have a major effect on the quantitative and qualitative aspect of activation of motor areas in humans.

Adult↗
PubMed1992

Supplementary and primary sensory motor area activity in Parkinson's disease. Regional cerebral blood flow changes during finger movements and effects of apomorphine.

We have measured with single-photon emission tomography the regional cerebral blood flow changes that occurred in the supplementary motor areas and in the primary sensory motor areas during sequential finger-to-thumb opposition movements of the right hand in seven akinetic patients with Parkinson's disease and in nine normal volunteers. Parkinsonian patients were studied before ("off" condition) and after a subcutaneous injection of apomorphine hydrochloride which was able to switch them "on" (on condition). In normal volunteers and parkinsonian patients in the on condition, regional cerebral blood flow significantly increased in the supplementary motor areas and in the contralateral primary sensory motor cortex but not in the ipsilateral primary sensory motor cortex. On the contrary, no significant regional cerebral blood flow change was observed in these areas in parkinsonian patients in the off condition. These results support the hypothesis that a functional cortical motor area deafferentation is involved in the pathophysiological makeup of akinesia and that this abnormality is reversed by dopaminergic drugs.

Aged↗
PubMed1991

Subcutaneous apomorphine increases regional cerebral blood flow in parkinsonian patients via peripheral mechanisms.

1. We have measured regional cerebral blood flow (rCBF) and motor function before and after the subcutaneous (s.c.) injection of apomorphine in parkinsonian patients deprived of their usual treatment for at least 48 h. 2. Nineteen patients, pretreated with domperidone (20 mg three times daily for 48 h), received a mean dose of 5.8 mg s.c. apomorphine. All patients switched 'on'. The mean motor score was significantly improved (-65%, P less than 0.01) but no significant change in rCBF was observed. 3. Seven other patients, not pretreated with domperidone, received a lower dose (0.3 mg) of s.c. apomorphine. No change in motor score was observed while the mean rCBF significantly increased (+12%, P less than 0.05). 4. We conclude that s.c. apomorphine increases rCBF in parkinsonian patients. This effect is independent of the central therapeutic effects of the drug. It is mediated by the stimulation of dopaminergic receptors of the cerebral vessels. These receptors are located outside the cerebral blood brain barrier and can be considered as 'peripheral' ones.

Aged↗
PubMed1991

Square wave jerks in parkinsonian syndromes.

The frequency of square wave jerks (SWJ) was compared in eight patients with progressive supranuclear palsy (PSP), 25 patients with multiple system atrophy or Parkinson's disease plus (MSA/PP), 85 patients with idiopathic Parkinson's disease (PD) and 20 age-matched normal volunteers. In the control group, the mean (SD) SWJ frequency (SWJ larger than 1 degree amplitude) was 2.3 (2.4)/min. Abnormal ocular fixation (SWJ frequency greater than 10/min) was observed in a large proportion of PSP patients (7/8) and of MSA/PP patients (16/25) but in few PD patients (13/85). In the group of PD patients with abnormal ocular fixation, freezing of gait, falls and instability were more severe than in the group of PD patients with normal fixation. The study of ocular fixation may help to differentiate PD clinically from other Parkinsonian syndromes. SWJ are probably not related to the central degeneration of the dopaminergic nigrostriatal pathway observed in PD.

Aged↗