Biomedical subjects

Jean Paul Nguyen

Publications and source records attributed to Jean Paul Nguyen.

4 recordsLinked to original sources

PubMed2002

Dopaminergic function and dopamine transporter binding assessed with positron emission tomography in Parkinson disease.

BACKGROUND: Measuring progression of Parkinson disease (PD) using positron emission tomography may help demonstrate the efficacy of neuroprotective treatments. To date, (18)F-dopa has been the gold standard to measure presynaptic dopaminergic function in PD, but this tracer might overestimate the rate of neuronal death in PD because its uptake also depends on dopamine turnover rather than exclusively on the density of dopaminergic terminals in the striatum. The latter might be assessed using newly developed ligands of the membrane dopamine transporter. OBJECTIVE: To compare the striatal uptakes of (18)F-dopa and (76)Br-FE-CBT, a dopamine transporter ligand, in patients with PD. PATIENTS AND METHODS: The striatal uptakes of (76)Br-FE-CBT and (18)F-dopa were compared using positron emission tomography in 10 patients with early PD and 8 with advanced PD. Correlation of uptakes with motor performance was investigated. RESULTS: The reduction in (76)Br-FE-CBT binding to 43% of control values was more severe than the reduction in (18)F-dopa uptake (63% of control values) in the putamen of patients with early PD. No significant difference was found between either tracer's uptake in the putamen of patients with advanced PD. Motor performance was highly correlated to (18)F-dopa uptake, whereas correlation to (76)Br-FE-CBT binding was weak. CONCLUSIONS: Uptake of (18)F-dopa may be up-regulated in early PD, suggesting a compensatory increase of dopamine synthesis in surviving dopaminergic terminals. Positron emission tomography dopamine transporter ligands and (18)F-dopa give complementary information on the presynaptic status of the nigrostriatal dopaminergic system and might be associated to investigate the efficacy of neuroprotective treatments in PD.

Aged↗

PubMed2002

Motor cortex stimulation in the treatment of deafferentation pain. I. Localization of the motor cortex.

MRI and electrophysiological techniques to localize the primary motor cortex (MC) were performed on patients considered for MC stimulation for the treatment of deafferentation pain. The representation and trajectory of the rolandic fissure (RF) were accurately localized by external cranial landmarks and radiopaque fiducials superimposed on oblique MRI sections. In addition, the scalp distribution of the corticocortical responses elicited by acute epidural stimulation [motor cortex (MC) in frontal and sensory cortex (SC) in parietal scalp regions], and analgesic responses at the topographical representation of the painful periphery elicited by subacute epidural stimulation were found to be simple and reliable procedures to localize MC, SC and RF.

Causalgia↗

PubMed1991

Central pain and thalamic hyperactivity: a single photon emission computerized tomographic study.

Five patients with central post-stroke pain (CPSP) accepted to be studied according to the following paradigm: a single photon emission computerized tomography (SPECT) using [123I]N-isopropyl-iodoamphetamine (IMP) was made in each patient 20 min following i.v. injection of IMP; during this time, the patients were stimulated in order to reproduce their spontaneous pain. Of the five patients, two had CPSP with hyperpathia following a stroke (with a lesion on CT scan involving the thalamo-cortical pathway in one and involving the thalamus in the other); two had CPSP following a stroke in the middle cerebral artery area, without hyperpathia; and the last patient suffered pain from algodystrophia following a fracture of the wrist. In the two cases with hyperpathia, SPECT demonstrated a contralateral relative hyperactivity in a central region corresponding to the thalamic area. This was not observed in the three other patients. In the two patients with hyperpathia, a second SPECT scan with stimulation of the contralateral pain-free arm did not demonstrate any hyperactivity in the thalamic area. These results suggest that a thalamic neuronal hyperactivity may characterize some hyperpathic syndromes and, in accordance with our previous results obtained in the rat, that the loss of inhibition on medial thalamic neurons may be a main feature of hyperpathia following certain cerebral stroke syndromes.

Aged↗

PubMedDate not supplied

[Motor cortex stimulation in the central pain syndrome].

We present a case of a 45-year-old male, treated with motor cortex stimulation (MCS). The procedure was performed in order to decrease symptoms of the central pain syndrome (CPS), which developed seven years earlier, after a left-side, cerebellum and brainstem ischemic stroke. The syndrome is defined as pain due to primary damage or dysfunction of the central nervous system. The pain was not sensitive to pharmacological and previous surgical interventions. During four months of follow-up after surgery with the use of MCS, 20% reduction of pain (Visual Analog Scale), withdrawal of narcotic and decrease of non-narcotic medications, ability to introduce rehabilitation and improvement of sleep were observed. No side effects were noticed. The procedure of electrode implantation to motor cortex is a relatively new treatment option in refractory central and neuropathic pain syndromes. The number of described procedures does not exceed 500 worldwide. The presented case is to our knowledge the first procedure of its type in Poland, giving hope to CPS patients, whose symptoms are otherwise difficult to treat.

Cerebral Infarction↗