scholarly journals The Effects of Pilocarpine in Patients with Orofacial Movement Disorder

2012 ◽  
Vol 37 (2) ◽  
pp. 107-112
Author(s):  
Sung-Hee Jeong ◽  
Soo-Min Ok ◽  
Joon-Young Huh ◽  
Myung-Yun Ko ◽  
Yong-Woo Ahn
Keyword(s):  
Movement Disorder ◽  
Orofacial Movement

Aberrant Sensorimotor Integration in Musicians' Cramp Patients

2003 ◽  
Vol 17 (4) ◽  
pp. 195-202 ◽  
Author(s):  
Vanessa K. Lim ◽  
John L. Bradshaw ◽  
Michael E.R. Nicholls ◽  
Ian J. Kirk ◽  
Jeff P. Hamm ◽  
...  
Keyword(s):  
Movement Disorder ◽  
Sensorimotor Cortex ◽  
Sensorimotor Integration ◽  
Group Interaction ◽  
Focal Dystonia ◽  
The Other ◽  
Alpha Power ◽  
Significant Group ◽  
Group Interactions

AbstractSimple tapping and complex movements (Luria finger apposition task) were performed unimanually and bimanually by two groups of professional guitarists while EEG was recorded from electrodes over the sensorimotor cortex. One group had a task-specific movement disorder (focal dystonia or musicians' cramp), while the other group did not (controls). There were no significant group interactions in the task-related power (TRPow) within the alpha range of 8-10Hz (mu1). In contrast, there was a significant group interaction within the alpha range of 10-12Hz (mu2); these latter frequencies are associated with task-specific sensorimotor integration. The significant group interaction included task (simple and complex) by hand (left, right, and both) by electrodes (10 electrodes over the sensorimotor areas). In the rest conditions, the alpha power (10-12Hz) was comparable between the groups; during movement, however, compared to the controls, patients demonstrated the greatest TRPow (10-12Hz) over all conditions. This was particularly evident when patients used their affected hand and suggests that patients with musicians' cramp have impaired task-specific sensorimotor integration.

GLUT1 deficiency in a child with a movement disorder

2008 ◽  
Vol 39 (05) ◽  
Author(s):  
A Bertsche ◽  
R Santer ◽  
D Vater ◽  
F Ebinger ◽  
D Rating ◽  
...  
Keyword(s):  
Movement Disorder ◽  
Glut1 Deficiency

Early plasmapheresis in 3 consecutive cases of choreo-athetotic movement disorder after HSV-1 encephalitis

2011 ◽  
Vol 42 (S 01) ◽  
Author(s):  
I Lanator ◽  
M Freilinger ◽  
D Csaicsich ◽  
R Seidl ◽  
MT Schmook
Keyword(s):  
Movement Disorder ◽  
Hsv 1

Functional Movement Disorder in a Family with PRRT2-Associated Paroxysmal Kinesigenic Dyskinesia

2014 ◽  
Vol 45 (S 01) ◽  
Author(s):  
D. Ebrahimi-Fakhari ◽  
K. Kang ◽  
U. Kotzaeridou ◽  
S. Schubert-Bast ◽  
J. Kohlhase ◽  
...  
Keyword(s):  
Movement Disorder ◽  
Functional Movement ◽  
Paroxysmal Kinesigenic Dyskinesia

Presentation of an Anti-NMDAR-Encephalitis with Focal Motor Seizures and Focal Movement Disorder

2014 ◽  
Vol 45 (S 01) ◽  
Author(s):  
A. Berger ◽  
L. Schmid ◽  
C. Betzler ◽  
C. Bien ◽  
K. Rostasy ◽  
...  
Keyword(s):  
Movement Disorder ◽  
Nmdar Encephalitis

FV 1031. Whole Exome Sequencing for Children with Dyskinetic Movement Disorder

2018 ◽  
Author(s):  
Yasemin Dincer ◽  
Michael Zech ◽  
Matias Wagner ◽  
Nikolai Jung ◽  
Volker Mall ◽  
...  
Keyword(s):  
Movement Disorder ◽  
Exome Sequencing ◽  
Whole Exome Sequencing ◽  
Whole Exome ◽  
Dyskinetic Movement

MRI in Movement Disorder Patients: "Hot cross bun" sign

2003 ◽  
Vol 49 (2) ◽  
pp. 85
Author(s):  
Seong Beom Koh ◽  
Byung Jo Kim ◽  
Min Kyu Park ◽  
Kun Woo Park ◽  
Nam Joon Lee ◽  
...  
Keyword(s):  
Movement Disorder

A glance on dystonias, how to recognize and handle them

2019 ◽  
pp. 22-29
Author(s):  
F. N. Mercan ◽  
E. Bayram ◽  
M. C. Akbostanci
Keyword(s):  
Differential Diagnosis ◽  
Movement Disorder ◽  
Age Of Onset ◽  
Clinical Manifestations ◽  
Body Part ◽  
Classification Model ◽  
Treatment Choices ◽  
Muscle Groups

Dystonia refers to an involuntary, repetitive, sustained, painful and twisting movements of the affected body part. This movement disorder was first described in 1911 by Hermain Oppenheim, and many studies have been conducted to understand the mechanism, the diagnosis and the treatment of dystonia ever since. However, there are still many unexplained aspects of this phenomenon. Dystonia is diagnosed by clinical manifestations, and various classifications are recommended for the diagnosis and the treatment. Anatomic classification, which is based on the muscle groups involved, is the most helpful classification model to plan the course of the treatment. Dystonias can also be classified based on the age of onset and the cause. These dystonic syndromes can be present without an identified etiology or they can be clinical manifestations of a neurodegenerative or neurometabolic disease. In this review we summarized the differential diagnosis, definition, classifications, possible mechanisms and treatment choices of dystonia.

scholarly journals Classic Ketogenic Diet and Modified Atkins Diet in SLC2A1 Positive and Negative Patients with Suspected GLUT1 Deficiency Syndrome: A Single Center Analysis of 18 Cases

Nutrients ◽  
2021 ◽  
Vol 13 (3) ◽  
pp. 840
Author(s):  
Jana Ruiz Herrero ◽  
Elvira Cañedo Villarroya ◽  
Luis González Gutiérrez-Solana ◽  
Beatriz García Alcolea ◽  
Begoña Gómez Fernández ◽  
...  
Keyword(s):  
Movement Disorder ◽  
Glucose Transporter ◽  
Deficiency Syndrome ◽  
Laboratory Assessment ◽  
Modified Atkins Diet ◽  
Atkins Diet ◽  
Glut1 Deficiency ◽  
Glut1 Deficiency Syndrome ◽  
The Impact

Background: Glucose transporter type 1 deficiency syndrome (GLUT1DS) is caused by mutations in the SLC2A1 gene and produces seizures, neurodevelopmental impairment, and movement disorders. Ketogenic dietary therapies (KDT) are the gold standard treatment. Similar symptoms may appear in SLC2A1 negative patients. The purpose is to evaluate the effectiveness of KDT in children with GLUT1DS suspected SLC2A1 (+) and (-), side effects (SE), and the impact on patients nutritional status. Methods: An observational descriptive study was conducted to describe 18 children (January 2009–August 2020). SLC2A1 analysis, seizures, movement disorder, anti-epileptic drugs (AEDS), anthropometry, SE, and laboratory assessment were monitored baseline and at 3, 6, 12, and 24 months after the onset of KDT. Results: 6/18 were SLC2A1(+) and 13/18 had seizures. In these groups, the age for debut of symptoms was higher. The mean time from debut to KDT onset was higher in SLC2A1(+). The modified Atkins diet (MAD) was used in 12 (5 SLC2A1(+)). Movement disorder improved (4/5), and a reduction in seizures >50% compared to baseline was achieved in more than half of the epileptic children throughout the follow-up. No differences in effectiveness were found according to the type of KDT. Early SE occurred in 33%. Long-term SE occurred in 10, 5, 7, and 5 children throughout the follow-up. The most frequent SE were constipation, hypercalciuria, and hyperlipidaemia. No differences in growth were found according to the SLC2A1 mutation or type of KDT. Conclusions: CKD and MAD were effective for SLC2A1 positive and negative patients in our cohort. SE were frequent, but mild. Permanent monitoring should be made to identify SE and nutritional deficits.

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