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JMD : Journal of Movement Disorders

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Original Article
Anticholinergic Agents Can Induce Oromandibular Dyskinesia
Hee-Young Shin, Won Tae Yoon, Won Yong Lee
J Mov Disord. 2009;2(2):69-71.
DOI: https://doi.org/10.14802/jmd.09018
  • 17,248 View
  • 70 Download
  • 2 Citations
AbstractAbstract PDF
Background and Purpose:

Oromandibular dyskinesia (OMD) can occur spontaneously or they can be induced by the conventional dopamine receptor antagonists. Anticholinergic medications have rarely been reported to cause OMD in parkinsonian or non-parkinsonian patients.

Methods:

We analyzed the clinical features of two parkinsonian and one non-parkinsonian patients who experienced OMD after anticholinergic medication.

Results:

Each patient of our cases developed oromandibular symptoms in the temporal regions that were related to the addition of anticholinergic agents, and the symptoms were relieved following the discontinuation of the causative anticholinergic drugs. In one of our case, levodopa alone did not cause dyskinesia but augmented dyskinesia associated with anticholinergics.

Conclusions:

Here we report two parkinsonian and one non-parkinsonian patients with OMD induced by the use of anticholinergic agents. In our cases, we could not find any other precipitating or actual secondary causes for the OMD symptoms in our patients. Furthermore, the fact that the OMD in our cases were ameliorated with cessation of anticholinergics suggests that it may be anticholinergic-induced.

Citations

Citations to this article as recorded by  
  • Impact of anticholinergic drugs withdrawal on motor function in patients with Parkinson’s disease
    Yasaman Saeedi, Maryam Ghadimi, Mohammad Rohani, Maziar Emamikhah, Gholamali Shahidi, Mehdi Moghaddasi, Seyed Amir Hassan Habibi
    Clinical Neurology and Neurosurgery.2021; 202: 106480.     CrossRef
  • Treatment of Tardive Dyskinesia: A General Overview with Focus on the Vesicular Monoamine Transporter 2 Inhibitors
    Nicki Niemann, Joseph Jankovic
    Drugs.2018; 78(5): 525.     CrossRef
Case Report
Painless Legs and Moving Toes as an Initial Presentation of Ischemic Stroke
Se Mi Oh, Won Tae Yoon, Ji Youn Kim, Hee-Young Shin, Won Yong Lee
J Mov Disord. 2009;2(1):40-42.
DOI: https://doi.org/10.14802/jmd.09010
  • 37,630 View
  • 92 Download
  • 3 Citations
AbstractAbstract PDF

Painless legs and moving toes is an unusual syndrome, which has not previously been reported as an initial presentation of ischemic stroke. We encountered a 78-year-old woman who developed dysarthria and involuntary movement of her left toes that was clinically regarded as painless legs and moving toes. These symptoms appeared abruptly and simultaneously as the initial symptoms of stroke, and improved gradually with conservative management by intravenous hydration for a month. We suggest that, in our case, a cortical brain lesion caused by ischemic stroke might be associated with the development of painless legs and moving toes.

Citations

Citations to this article as recorded by  
  • Painful legs and moving toes syndrome
    Hiroki Tamura, Kosuke Ishizuka, Kiyoshi Shikino, Masatomi Ikusaka
    BMJ Case Reports.2021; 14(3): e240692.     CrossRef
  • Movement Disorders Following Cerebrovascular Lesions: Etiology, Treatment Options and Prognosis
    Do-Young Kwon
    Journal of Movement Disorders.2016; 9(2): 63.     CrossRef
  • Painful legs and moving toes syndrome in a 16-year-old girl
    Seung Soo Kim, Yong Seung Hwang, Young Chang Kim
    Korean Journal of Pediatrics.2016; 59(9): 381.     CrossRef
Original Article
Reliability of Serum Anti-thyroid Antibody Screening in the Diagnosis of Parkinson’s Disease and Multiple System Atrophy
Taek-Jun Lee, Hee-Young Shin, Won Tae Yoon, Won Yong Lee
J Mov Disord. 2008;1(2):75-81.
DOI: https://doi.org/10.14802/jmd.08014
  • 32,991 View
  • 185 Download
AbstractAbstract PDF
Backgrounds:

Ataxia associated with Hashimoto’s thyroiditis autoantibodies has been reported as acquired cerebellar ataxia. However, relationship between anti-thyroid antibodies and cerebellar ataxia has not been clarified yet.

Objectives:

We aimed to analysis the relibility of serum anti-thyroid antibodies screening in the diagnosis of Parkinson’s disease (PD) and multiple system atrophy (MSA).

Method:

We enrolled 105 patients with clinically diagnosed PD and 75 patients with probable MSA. Patients with PD were classified into 70 patients with early PD (Hoehn & Yahr stage I to II) and 35 patients with late PD (Hoehn & Yahr stage III to IV). In MSA, 28 patients were classified as MSA-p (parkinsonism predominant) and 47 MSA-c (cerebellar predominant). For analysis of thyroid function, serum free triiodothyronine (T3), free thyroxine (T4), anti-thyroglobuline (TG) antibodies and anti-microsomal antibodies were measured. Cut-off level for abnormal titers of anti-thyroid antibodies were defiend as above 100 U/ml.

Results:

Abnormally high titer of serum anti-TG antibodies and anti-microsomal antibodies was more frequently observed in MSA than in PD (p =0.001 and 0.003, respectively). However, there was no significant difference in the frequency of abnormal titer either between MSA-c and MSA-p (p>0.05) nor between early PD and late PD (p>0.05). Among clinical parameters, only ataxia was correlated with both titer of anti-TG antibody and anti-microsomal antibody (p=0.007 and 0.002, respectively).

Conclusion:

These results suggest that high titer of anti-thyroid antibodies may be associated with MSA rather than PD and screening of serum anti-thyroid antibodies may be helpful for discrimiation of PD from MSA. However, anti-thyroid antibodies screening may not be helpful to differentiate MSA-c from MSA-p.


JMD : Journal of Movement Disorders