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Biomedical subjects

François Vingerhoets

Publications and source records attributed to François Vingerhoets.

11 recordsLinked to original sources

Does subthalamic nucleus deep brain stimulation really improve quality of life in Parkinson's disease?

We investigated the impact of subthalamic nucleus (STN) deep brain stimulation (DBS) on quality of life (QOL) in patients with advanced Parkinson's disease, as self-assessed before and after surgery by completing the Parkinson's Disease Questionnaire (PDQ39). In addition to this prospective evaluation, we asked patients postoperatively to evaluate their preoperative QOL. In the prospective assessment, results showed that patients perceived a general improvement of QOL after the STN DBS. However, when evaluated retrospectively, they tended to overestimate their preoperative functioning, therefore obscuring the improvement found prospectively. This observation highlights the impact of the method used on obtained results when assessing the effects of STN DBS.

Activities of Daily Living↗

[Novel brain stimulation techniques: therapeutic perspectives in psychiatry].

Recent advances have allowed the development of new physical techniques in neurology and psychiatry, such as Transcranial Magnetic Stimulation (TMS), Vagus Nerve Stimulation (VNS), and Deep Brain Stimulation (DBS). These techniques are already recognized as therapeutic approaches in several late stage refractory neurological disorders (Parkinson's disease, tremor, epilepsy), and currently investigated in psychiatric conditions, refractory to medical treatment (obsessive-compulsive disorder, resistant major depression). In Paralell, these new techniques offer a new window to understand the neurobiology of human behavior.

Deep Brain Stimulation↗

Role of dopaminergic treatment in dopamine receptor down-regulation in advanced Parkinson disease: a positron emission tomographic study.

BACKGROUND: In patients with advanced Parkinson disease (PD) who are undergoing long-term treatment with a dopaminergic medication, a down-regulation of striatal dopamine D2 receptor expression has been demonstrated and interpreted as a consequence of either the disease itself or dopaminergic drug administration. OBJECTIVE: To compare, using positron emission tomography, the striatal binding of raclopride carbon C 11, a dopamine D2 receptor ligand, in PD patients who completely discontinued dopaminergic therapy (off drug) with that in PD patients who continued receiving dopaminergic therapy (on drug) after undergoing subthalamic nucleus stimulation. MAIN OUTCOME MEASURES: The positron emission tomographic data were acquired in off-stimulation and, for 12 hours, off-medication conditions. Five off-drug PD patients, 7 on-drug PD patients, and 8 healthy subjects participated. RESULTS: In off-drug PD patients, the putaminal raclopride C 11 binding was 24% higher than in on-drug PD patients. The same tendency was noted for the caudate nucleus, but was not significant (P=.07). Compared with control subjects, the putaminal raclopride C 11 binding was increased by 21% in off-drug and was normal in on-drug PD patients. Compared with controls, the caudate raclopride C 11 binding was reduced by 23% in on-drug and was normal in off-drug PD patients. Further analysis using statistical parametric mapping showed a significant increase of binding bilaterally in the caudate nucleus and putamen in off-drug compared with on-drug PD patients (P=.002 at cluster level). CONCLUSIONS: The down-regulation of dopamine D2 receptors probably relates to the long-term and intermittent administration of dopaminergic treatments rather than to disease progression. This phenomenon is reversed by the complete withdrawal of dopaminergic drugs. Furthermore, an up-regulation of putaminal dopamine D2 receptors is demonstrated in late-stage PD after dopaminergic drug withdrawal.

Aged↗

Spinal cord lesion after long-term intrathecal clonidine and bupivacaine treatment for the management of intractable pain.

Long-term intrathecal drug administration using implanted pumps is increasingly used in the treatment of chronic refractory pain [Anderson and Burchiel 1999, Neurosurgery 44 (1999) 289; Krames 2002, Best Pract Res Clin Anaesthesiol 16 (2002) 619; Wallace 2002, Neurology 59 (2002) S18]. Extensive clinical experience over the last 15 years suggests that in selected cases the technique is safe, although infections, system malfunction and drug-related complications have been reported. In most cases, drug-related spinal cord injuries have resulted from the compression of a spinal inflammatory mass or abcess rather than from a direct neurotoxic effect. We report on a case of toxic spinal cord lesion occurring after more than 3 years of uneventful continuous infusion of a mixture of bupivacaine and clonidine.

Analgesia, Epidural↗

Acute infarction limited to the lenticular nucleus: clinical, etiologic, and topographic features.

BACKGROUND: Chronic diseases involving the putamen and globus pallidus induce parkinsonism and other movement disorders. Sensory and motor dysfunction from deep middle cerebral artery infarction is usually due to an involvement of the internal capsule. The clinical picture associated with isolated infarction of the lenticular nucleus is less well established. OBJECTIVE: To analyze clinical features, topographic correlations, and cause of purely lenticular ischemic infarction. PATIENTS AND METHODS: We reviewed 820 consecutive patients with deep hemispheral infarct included in the Lausanne Stroke Registry between 1986 and 1998 and selected those with isolated lenticular involvement on computed tomography or magnetic resonance imaging. RESULTS: Thirteen patients had pure lenticular infarction. All had faciobrachiocrural hemisyndrome, while none showed acute or delayed parkinsonism or abnormal movement. Nine patients had a lesion restricted to the putamen. Two of them had ataxic motor hemisyndrome and 7 had sensorimotor hemisyndrome (with ataxia in 4, left hemineglect in 1, and deep pain in the arm and leg in 1). Four patients had a lesion of putamen and globus pallidus externus. Three of them had motor hemisyndrome (with nonfluent aphasia in 2 and ataxia in 1) and 1 had ataxic sensorimotor hemisyndrome. All infarcts were in the territory of the medial perforating branches of the medial cerebral artery. Presumed cause of stroke was small-artery disease in 5, artery-to-artery embolism in 4, cardioembolism in 3 and undetermined in 1. CONCLUSIONS: Acute lenticular infarction induces mainly hemiparesis but no movement disorder. Associated sensory deficits, aphasia, and hemineglect underline clinically the function of the lenticular nucleus in connection with the prefrontal, temporal, and parietal cortices.

Acute Disease↗

Subthalamic nucleus deep brain stimulation for Parkinson's disease: magnetic resonance imaging targeting using visible anatomical landmarks.

BACKGROUND: The aim of the present study was to validate a magnetic resonance imaging (MRI) visual procedure to target the subthalamic nucleus (STN) based on surrounding anatomical landmarks. METHODS: 31 consecutive bilaterally implanted parkinsonian patients were included in this study. After identification of the anterior commissure (AC), posterior commissure (PC) and midcommissural point on a three-dimensional T1-weighted sequence, inversion recovery (IR) T2-weighted coronal slices were performed orthogonal to the AC-PC line. On the slice showing the anterior pole of the red nucleus (RN), the target was placed in the inferolateral portion of the subthalamic zone, limited superiorly by the thalamus, laterally by the internal capsule, inferiorly by the substantia nigra and medially by the midline. The distribution of the targets was analyzed in the AC-PC referential. RESULTS: The mean target coordinates were as follows: anteroposterior (AP) = -2.54 mm (+/-1.37 mm), lateral (LAT) = 12.03 mm (+/-0.91 mm) and vertical (VERT) = -6.10 mm (+/-1.52 mm) for the right side, and AP = -2.65 mm (+/-1.36 mm), LAT = -11.97 mm (+/-1.30 mm) and VERT = -5.89 mm (+/-1.52 mm) for the left side. They projected in the inferior portion of the STN on the Schaltenbrand and Wahren atlas [Stuttgart, Thieme, 1977]. CONCLUSION: Identification of the anterior pole of the RN and the subthalamic zone on coronal IR T2-weighted MRI performed orthogonal to the AC-PC line provides a precise visual procedure to target the STN.

Electric Stimulation Therapy↗

Persistence of mild parkinsonism 4 months after liver transplantation in patients with preoperative minimal hepatic encephalopathy: a study on neuroradiological and blood manganese changes.

Pallidal hyperintensity at magnetic resonance imaging (MRI) correlates to blood manganese (Mn) levels and parkinsonian signs in patients with cirrhosis. Similarly, metabolite changes in the basal ganglia (BG) at proton spectroscopy are related to these neurological signs. The evolution of these abnormalities after liver transplantation (OLT) is incompletely described. We evaluated 14 unselected consecutive patients with cirrhosis (minimal hepatic encephalopathy [HE] n=8, no HE n=6) before and 4 months after successful OLT for the evolution of parkinsonism using a validated scale (the United Parkinson's Disease Rating Scale, or UPDRS). Pallidal intensity at MRI, spectroscopic changes in the BG at magnetic resonance spectroscopy (MRS), and whole blood manganese concentrations were measured. After OLT in patients with preoperative minimal HE, the UPDRS scores improved, but mild parkinsonism persisted (16.1+/-3.6 to 6.2+/-4.8, P<0.05). Pallidal hyperintensity remained abnormal in 5/8 of cases, but spectroscopic changes normalized in all patients. Blood Mn remained elevated in 4/6 patients. In patients without HE, UPDRS values remained negligible (2.42+/-1.5 to 2.5+/-1.4). Pallidal hyperintensity normalized in 7/8 patients and spectroscopic changes normalized in all patients. Blood Mn remained elevated in 5/6 patients. Four months after successful OLT, patients with preoperative minimal HE and severe pallidal hyperintensity showed persistent mild parkinsonism. The role of blood manganese determination appears limited in the monitoring of MRI and parkinsonian signs changes after OLT.

Adult↗