Biomedical subjects

Reiner Benecke

Publications and source records attributed to Reiner Benecke.

22 records · Page 2Linked to original sources

PubMed2002

Deep brain stimulation for dystonia: patient selection and evaluation.

Deep brain stimulation (DBS) for dystonia still needs to be considered investigational, because there are no controlled studies for this indication, the optimal target point is uncertain, and long-term effects are unknown. The striking improvement of levodopa-induced dyskinesias in Parkinson's disease by deep brain stimulation of the internal pallidum has encouraged the use of this therapy for generalized and severe segmental dystonia in children and adults. Single case and small cohort studies have reported impressive efficacy of pallidal DBS in patients with primary dystonia, especially DYT1 mutation carriers, but results in secondary dystonia are less conclusive. This article discusses the different factors influencing patient selection for surgical treatment and describes standardized methods and the caveats for clinical documentation of treatment results in dystonia.

Clinical Protocols↗

PubMed2002

Botulinum toxin type B for treatment of axillar hyperhidrosis.

Recently, botulinum toxin type B (BT-B) became commercially available for treatment of cervical dystonia. It is the aim of this study to explore its use for treatment of bilateral axillar hyperhydrosis (HH). For this we directly compared the antihyperhydrotic effect of BT-B (NeuroBloc)/MyoBloc) with that of botulinum toxin type A (BT-A) (Botox). 9 patients (HD group) received BT-A 100MU unilaterally and BT-B 4000MU contralaterally. 10 patients (LD group) received BT-A 100MU and BT-B 2000MU. All patients were blinded as to which preparation was used in which side. All patients except one reported excellent HH improvement in both axillae. None of the patients had residual HH on clinical examination. The duration of HH improvement until first recurrence in the HD group was 16.0 +/-4.3 weeks in the BT-A treated axillar and 16.4 +/-4.5 weeks in the BT-B treated axillae (Wilcoxon rank-sum test, p = 0.336). In the LD group it was 16.4 +/-5.3 weeks in the BT-B treated axillae and 17.1 +/-5.7 weeks in the BT-A treated axillae (Wilcoxon rank-sum test, p = 0.059). There was also no difference in the duration of HH improvement between the axillae treated with BT-B 4000MU and BT-B 2000MU (Wilcoxon rank-sum test, p = 0.712). 5 out of 9 patients in the HD group (chi-square test, p = 0.025) and 7 out of 10 patients in the LD group (chi-square test, p = 0.008) reported more application discomfort in the BT-B treated axillae. In 6 out of 9 patients in the HD group (chi-square test, p = 0.014) and in 6 out of 10 patients in the LD group (chi-square test, p = 0.014) the onset of HH improvement appeared earlier in the BT-B treated axillae. One patient in the HD group reported dryness of the mouth and eyes and accomodation difficulties.BT-B is a safe and efficient treatment for axillar HH. Doses of BT-B 2000MU per axilla seem sufficient indicating a conversion factor between BT-A and BT-B in the order of 1:20. With a conversion factor for cervical dystonia in the order of 1:40 the autonomic nervous system seems to be relatively more sensitive to BT-B than to BT-A compared with the motor system.

Adult↗

PubMed2002

Clinical features and laboratory findings for differentiating parkinsonian syndromes.

Most clinicians and researchers still accept idiopathic Parkinson's disease as a disease entity, although the identification of several genes or loci responsible for certain inherited forms of Parkinson's disease have provided arguments for a clinical heterogeneity of this disorder. The here proposed new classification of syndromes and diseases which show a parkinsonian syndrome in isolation or in combination with other symptoms divides patients into groups based on a set of rules mainly on a clinicopathological basis. It illustrates the current state of the art and will eventually be replaced due to an increase in the knowledge of the pathophysiological basis of these diseases. According to this classification, the crucial clinical features and laboratory findings are reviewed. The report will mainly concentrate on parkinsonian syndromes in degenerative diseases.

Diagnosis, Differential↗

PubMed2002

Early diagnosis of Parkinson's disease.

In idiopathic Parkinson's disease (IPD) approximately 60 % of the nigrostriatal neurons of the substantia nigra (SN) are degenerated before neurologists can establish the diagnosis according to the widely accepted clinical diagnostic criteria. It is conceivable that neuroprotective therapy starting at such an 'advanced stage' of the disease will fail to stop the degenerative process. Therefore, the identification of patients at risk and at earlier stages of the disease appears to be essential for any successful neuroprotection. The discovery of several genetic mutations associated with IPD raises the possibility that these, or other biomarkers, of the disease may help to identify persons at risk of IPD. Transcranial ultrasound have shown susceptibility factors for IPD related to an increased iron load of the substantia nigra. In the early clinical phase, a number of motor and particularly non-motor signs emerge, which can be identified by the patients and physicians years before the diagnosis is made, notably olfactory dysfunction, depression, or 'soft' motor signs such as changes in handwriting, speech or reduced ambulatory arm motion. These signs of the early, prediagnostic phase of IPD can be detected by inexpensive and easy-to-administer tests. As one single instrument will not be sensitive enough, a battery of tests has to be composed measuring independent parameters of the incipient disease. Subjects with abnormal findings in this test battery should than be submitted to nuclear medicine examinations to quantify the extent of dopaminergic injury and to reach the goal of a reliable, early diagnosis.

3-Iodobenzylguanidine↗