Clinical characteristics and topography of lesions in movement disorders due to thalamic lesions

Lehericy, Stéphane; Grand, Sylvie; Pollak, Pierre; Poupon, Fabrice; Bas, J.F. Le; Limousin, Patricia; Jedynak, Piotr; Marsault, C.; Agid, Yves; Vidailhet, Marie

doi:10.1212/wnl.57.6.1055

Cited by 123 publications

(73 citation statements)

References 60 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…33,34 That said, the role of the thalamus in dystonia is by no means clear in that lesions in this area can also produce dystonic manifestations in both humans and experimental animal models. 35 Substantial dopaminergic input to the human ventral thalamus has been recognized. 36Ϫ38 In primates, DAT-positive terminals are evident at thalamic interneurons, 38 which are mainly inhibitory.…”

mentioning

confidence: 99%

Abnormal striatal and thalamic dopamine neurotransmission

Carbon

Niethammer²,

Peng³

et al. 2009

Neurology

118

View full text Add to dashboard Cite

Objective: To determine whether changes in D 2 receptor availability are present in carriers of genetic mutations for primary dystonia. Methods:Manifesting and nonmanifesting carriers of the DYT1 and DYT6 dystonia mutations were scanned with [11 C] raclopride (RAC) and PET. Measures of D 2 receptor availability in the caudate nucleus and putamen were determined using an automated region-of-interest approach.Values from mutation carriers and healthy controls were compared using analysis of variance to assess the effects of genotype and phenotype. Additionally, voxel-based whole brain searches were conducted to detect group differences in extrastriatal regions.Results: Significant reductions in caudate and putamen D 2 receptor availability were evident in both groups of mutation carriers relative to healthy controls (p Ͻ 0.001). The changes were greater in DYT6 relative to DYT1 carriers (Ϫ38.0 Ϯ 3.0% vs Ϫ15.0 Ϯ 3.0%, p Ͻ 0.001). By contrast, there was no significant difference between manifesting and nonmanifesting carriers of either genotype. Voxel-based analysis confirmed these findings and additionally revealed reduced RAC binding in the ventrolateral thalamus of both groups of mutation carriers. As in the striatum, the thalamic binding reductions were more pronounced in DYT6 carriers and were not influenced by the presence of clinical manifestations. Conclusions:Reduced D 2 receptor availability in carriers of dystonia genes is compatible with dysfunction or loss of D 2 -bearing neurons, increased synaptic dopamine levels, or both. These changes, which may be present to different degrees in the DYT1 and DYT6 genotypes, are likely to represent susceptibility factors for the development of clinical manifestations in mutation carriers. Neurology GLOSSARY ANOVA ϭ analysis of variance; BFM ϭ Burke-Fahn-Marsden; CN ϭ caudate nucleus; FWE ϭ family-wise error rate; GPe ϭ external pallidum; GPi ϭ interal pallidum; RAC ϭ raclopride; ROI ϭ region of interest; SOR ϭ striato-occipital ratio; THX ϭ trihexyphenidyl; VL ϭ ventrolateral tier nuclei.Multiple lines of evidence support the role of altered striatal DA neurotransmission in primary dystonia. 1,2 Nonetheless, imaging studies have revealed only minimal reductions in striatal D 2 receptor binding in patients with idiopathic dystonia 3,4 and in nonmanifesting carriers of the DYT1 dystonia mutation.5 Indeed, similar reductions have been described in DYT1 dystonia patients at postmortem.1 It is not known whether similar abnormalities are also present in primary dystonia associated with other genetic mutations.Experimental models of dystonia have yielded varied results with regard to the striatal DA dynamics. Increased striatal DA turnover was found in a transgenic murine DYT1 model regardless of behavioral phenotype. 6,7 However, in this model, striatal DA levels were reduced

show abstract

mentioning

confidence: 99%

Abnormal striatal and thalamic dopamine neurotransmission

Carbon

Niethammer²,

Peng³

et al. 2009

Neurology

118

View full text Add to dashboard Cite

show abstract

“…Lesion studies in humans indicate that dystonia is mainly observed after lesions of the caudal motor thalamus (Vc, VIM) but not of the rostral pallidal segment (Vop) (52,53). In monkey, the motor thalamus is a complex structure encompassing several regions (54).…”

Section: Lessons Form Primate Models Of Dystonia: the Physiological Amentioning

confidence: 99%

Dystonia Pathophysiology: A Critical Review

Burbaud¹

2012

Dystonia - The Many Facets

View full text Add to dashboard Cite

“…The vascular territory of the lesion suggests a cardiac source of embolism. [2][3][4] Lipomas are benign nonmyxomatous neoplasms of the heart that normally cause no symptoms and their diagnosis is often accidental. [5][6][7] They represent 10% of the overall cardiac tumor masses arising from cardiac tissue and they are most frequently located in the right atrium.…”

Section: Brief Communicationsmentioning

confidence: 99%

“…2,3 Its etiological relationship with stroke is not well established. We describe the case of a thalamic stroke probably caused by paradoxical embolism from a right atrial lipoma through a patent foramen ovale.…”

mentioning

confidence: 99%

Anterior Thalamic Infarction as Initial Manifestation of a Right Atrial Lipoma

Erro

Ajuria

Olaz

et al. 2009

Can. J. Neurol. Sci

View full text Add to dashboard Cite

Cardiac tumors are an infrequent source of embolism to the brain in young adults. Myxomas are the most common among them and they are mainly located in the left atrium.1 Cardiac lipomas are a very rare benign neoplasm of the heart usually located in the right atrium.2,3 Its etiological relationship with stroke is not well established. We describe the case of a thalamic stroke probably caused by paradoxical embolism from a right atrial lipoma through a patent foramen ovale. CASE REPORTA 46-year-old male with mild hypertension, presented with speech and behavioral alterations first noticed on awakening without a previous Valsalva manoeuvre. On admission his blood pressure was 150/90 mm Hg, with a pulse of 70 beats/min and O 2 saturation of 97%. He was apyretic and cardiac and cervical auscultation was unremarkable. On neurologic examination, a non-fluent dysphasia with word finding difficulties, right facial paresis and a left Horner's syndrome was observed. He also presented mild right hemiparesis and myoclonic-dystonic movements in lower limbs (NIHSS 7). Cervical and Transcranial Doppler (TCD) were normal. Cranial computerized tomography was normal. A cranial magnetic resonance (MR) demonstrated on diffusion sequences the presence of an acute non-hemorrhagic infarction involving the anterior area of the left thalamus ( Figure 1A). Perfusion MR sequences and cerebral magnetic angioresonance were normal. The patient was admitted to the stroke unit. Conservative treatment was initiated. No arrhythmia was registered during hospitalization. Duplex sonography excluded atherosclerotic lesions in the carotid arteries. The next day, a right to left massive shunt was found on TCD bubble study ( Figure 1B). This test was performed using agitated saline as a contrast agent. Thrombophilic screening, neoplastic markers and autoimmune assays were negative. Transthoracic and transesophageal echocardiograms (TEE) were performed showing a mobile mass of homogeneous density attached to the free wall of the right atrium ( Figure 1C). No other cardioembolic lesions such as aortic plaques or dysfunctional left ventricle were found. The mass could be optimally assessed by cardiac MR as a well defined, slightly lobulated and homogeneous lesion, strongly hyperintense on T1 sequences, with low signal intensity on Fat-suppressed sequences (T2 STIR) and without contrast enhancement after gadolinium administration ( Figure 1D), highly suggestive of a lipoma. A patent foramen ovale (PFO) without associated aneurysmal septum could also be seen on TEE. The mass and the foramen ovale were surgically removed THE CANADIAN JOURNAL OF NEUROLOGICAL SCIENCES 379

show abstract

Clinical characteristics and topography of lesions in movement disorders due to thalamic lesions

Cited by 123 publications

References 60 publications

Abnormal striatal and thalamic dopamine neurotransmission

Abnormal striatal and thalamic dopamine neurotransmission

Dystonia Pathophysiology: A Critical Review

Anterior Thalamic Infarction as Initial Manifestation of a Right Atrial Lipoma

Contact Info

Product

Resources

About