This article requires a subscription to view the full text. If you have a subscription you may use the login form below to view the article. Access to this article can also be purchased.
Abstract
We report the transcranial sonography (TCS) findings of the basal ganglia in 86 patients with dystonic disorders including idiopathic dystonia (facial, cervical, upper limb, and generalized dystonia), drug-induced tardive dystonia, dopa-responsive dystonia, and kinesigenic dystonia. The TCS was focused on alterations of the lenticular, caudate, raphe nuclei, and the thalamus. Seventy-five percent of patients with idiopathic cervical and 83% of those with idiopathic upper limb dystonia had a hyperechogenic lesion of the middle segment of the lenticular nucleus on the side opposite to the clinical dystonic symptoms. The ipsilateral side was also affected in 20%. In facial dystonia, only one-third of the patients revealed lenticular nucleus lesions. The mean area of the lenticular nucleus lesion opposite to the clinically affected side was 30 mm2 in cervical dystonia, 17 mm2 in upper limb dystonia, and 7.5 mm2 in facial dystonia. These lenticular abnormalities were significantly more frequent (p < 0.001) and their areas were significantly greater (p < 0.001) compared with a control group of 50 patients afflicted with radiculopathy. There was a significant correlation of the severity of symptoms with the intensity of lenticular nucleus hyperechogenicity in patients with cervical and upper limb dystonia (p < 0.05). Increased caudate nucleus echogenicity was present in 20% of patients with cervical and upper limb dystonia, mostly contralateral to the clinically affected side, and raphe abnormalities were present in 7% of all patients with idiopathic dystonia. In contrast, there were no abnormalities of the lenticular nucleus or thalamus in nonidiopathic dystonias. We conclude that idiopathic dystonia is associated with lesions in the basal ganglia, particularly the lenticular nucleus, that can be visualized by TCS. An alteration of the basal ganglia matrix may be the pathologic basis of idiopathic dystonia with secondary affliction of striatopallidothalamic pathways.
NEUROLOGY 1996;47: 1284-1290
- Copyright 1996 by Advanstar Communications Inc.
AAN Members
We have changed the login procedure to improve access between AAN.com and the Neurology journals. If you are experiencing issues, please log out of AAN.com and clear history and cookies. (For instructions by browser, please click the instruction pages below). After clearing, choose preferred Journal and select login for AAN Members. You will be redirected to a login page where you can log in with your AAN ID number and password. When you are returned to the Journal, your name should appear at the top right of the page.
AAN Non-Member Subscribers
Purchase access
Letters: Rapid online correspondence
REQUIREMENTS
You must ensure that your Disclosures have been updated within the previous six months. Please go to our Submission Site to add or update your Disclosure information.
Your co-authors must send a completed Publishing Agreement Form to Neurology Staff (not necessary for the lead/corresponding author as the form below will suffice) before you upload your comment.
If you are responding to a comment that was written about an article you originally authored:
You (and co-authors) do not need to fill out forms or check disclosures as author forms are still valid
and apply to letter.
Submission specifications:
- Submissions must be < 200 words with < 5 references. Reference 1 must be the article on which you are commenting.
- Submissions should not have more than 5 authors. (Exception: original author replies can include all original authors of the article)
- Submit only on articles published within 6 months of issue date.
- Do not be redundant. Read any comments already posted on the article prior to submission.
- Submitted comments are subject to editing and editor review prior to posting.
