ArticleJournal of neurology2011
Basal ganglia hyperechogenicity does not distinguish between patients with primary dystonia and healthy individuals.
Article in Journal of neurology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 1 of them a synthesis that pooled it.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
6 citing papers in PubMed, 1 synthesis or guideline pooled it, 9 citations in OpenAlex.
- Pooled it
- Striatal hyperechogenicity as an ultrasound imaging marker for prodromal X-linked dystonia-parkinsonism.NPJ Parkinson's disease · 2026Article
- An unusual gait disorder at the Emergency Department: role of the quantitative assessment of parenchymal transcranial Doppler sonography.Quantitative imaging in medicine and surgery · 2021Article
- Transcranial Sonography in Mitochondrial Membrane Protein-Associated Neurodegeneration.Clinical neuroradiology · 2018Article
- Sonographic Alteration of Basal Ganglia in Different Forms of Primary Focal Dystonia: A Cross-sectional Study.Chinese medical journal · 2016Article
- Echogenicity of basal ganglia structures in different Huntington's disease phenotypes.Journal of neural transmission (Vienna, Austria : 1996) · 2015Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Transcranial sonography (TCS) of the basal ganglia is a non-invasive tool to study movement disorders. Very few studies have addressed the question of whether TCS may detect specific echofeatures in patients with primary dystonia. The basal ganglia including the substantia nigra (SN) and the ventricular system were investigated by TCS in 84 primary dystonia patients and 43 neurologically healthy controls. Any hyperechogenicity of the lenticular nucleus was present in 57.5% of the patients and in 50.0% of the controls (p = 0.453). While marked hyperechogenicity was more frequently present in the patients (17.8 vs. 7.9%), this difference was not significant (p = 0.227). No differences in the occurrence of hyperechogenicity were detectable either in the caudate nucleus (21.6 vs. 39.5%, p = 0.122) or the thalamus (4.1 vs. 0%, p = 0.199). Marked hyperechogenicity of the caudate nucleus was rare in dystonia (4.1%) and absent in controls. There was no relationship between the side of basal ganglia hyperechogenicity and the clinically affected side of cervical dystonia. The area of SN echogenicity was similar in patients and controls (0.19 ± 0.14 vs. 0.20 ± 0.13 cm(2)), but correlated negatively with increasing disease duration in the dystonia patients (ρ = -0.257, p = 0.028). Width of the third ventricle correlated with increasing age (ρ = 0.511, p = 0.000) and, in patients, with disease duration (ρ = 0.244, p = 0.034) and severity of cervical dystonia (ρ = 0.281, p = 0.038). No characteristic abnormalities were found in the basal ganglia of primary dystonia patients. It remains to be explored whether this is due to a true absence of signal alterations in the basal ganglia of dystonia patients or to limitations of the current technology used.
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