Comparison of transcranial sonography, magnetic resonance imaging, and single photon emission computed tomography findings in idiopathic spasmodic torticollis

Abstract

Various lines of evidence suggest that the basal ganglia and thalamus are involved in the pathogenesis of idiopathic dystonia, but unfortunately neuroradiological and pathological data are sparse and controversial. In this study, we have examined 10 patients with spasmodic torticollis by neuroimaging techniques, including transcranial sonography (TS; n = 10), conventional (n = 10) and diffusion-weighted (n = 5) magnetic resonance imaging (MRI), and single photon emission computed tomography (SPECT; n = 10), employing [123I]iodobenzamide (IBZM) as a ligand with a high affinity to the D2 receptor. In seven patients, TS showed small hyperechogenic lesions in the medial segments of the lentiform nucleus contralateral to the side of head deviation. In accordance with the site of TS abnormalities, diffusion-weighted MRI displayed a hyperintense lesion in only one patient, while standard MRI of this area was normal in all patients. SPECT revealed a slight but statistically nonsignificant reduction of IBZM tracer uptake in an area corresponding to the dorsal portions of the striatum in 9 of the 10 patients. TS findings support the hypothesis that structural alternations of the pallidothalamic circuit contralateral to the side of head deviation are involved in the pathogenesis of idiopathic spasmodic torticollis. TS may be more sensitive in detecting basal ganglia alterations than MRI.

Reduced Serum Ceruloplasmin Levels in Cervical Dystonia

“…Previous studies have repeatedly demonstrated disturbances of copper metabolism in primary dystonia by transcranial ultrasound [3,4,5], leukocyte analysis [6], and neurochemical analysis of trace metals and proteins in the brain tissue [7,8]. The findings were also reproduced in post-surgical secondary dystonia [9], implying the presence of subjects susceptible to dystonia, although the copper gene might be irrelevant by itself to the pathogenesis of dystonia [10].…”

Basal ganglia hyperechogenicity does not distinguish between patients with primary dystonia and healthy individuals

“…After the original publication of two TCS studies on dystonia in the mid-90s, this is currently the only report addressing the question of whether TCS may detect (a) specific hyperechogenic areas in the basal ganglia and thalamus, and (b) size changes of the ventricular system and the aSN in patients with primary dystonia [2,14].…”

“…This echofeature represents a potential vulnerability marker for the development of a nigral dysfunction [5,6]. Apart from the SN, increased hyperechogenicity of the lenticular nucleus (LN) has been described in patients with primary dystonia [2,14]. However, little is known about the underlying cause of TCS hyperechogenicity in the LN.…”

Update on Transcranial Sonography Applications in Movement Disorders

“…By using TCS, a hyperechogenicity of the LN can be detected in up to 75% of patients with idiopathic cervical dystonia or upper-limb dystonia [84]. It can be shown that an increased echogenicity of the SN in only 31% of patients with facial dystonia whereas this echo feature is not usually seen in tardive dystonia [84].…”

“…It can be shown that an increased echogenicity of the SN in only 31% of patients with facial dystonia whereas this echo feature is not usually seen in tardive dystonia [84]. Consequently, this ultrasound feature might be useful in distinguishing idiopathic dystonia from tardive or psychogenic dystonias (Figure 4 C) [24].…”