G Kranz1, E A Shamim, P T Lin, G S Kranz, B Voller, M Hallett. 1. Human Motor Control Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD, USA. gottfried.kranz@meduniwien.ac.at
Abstract
BACKGROUND: Traditionally, benign essential blepharospasm (BEB) is considered a disorder caused by basal ganglia dysfunction. Electrophysiologic and brain imaging studies suggest pathologic changes in excitability in the primary motor cortex (MC), anterior cingulate (AC), and secondary motor areas, such as premotor (PMC) and supplementary motor cortices (SMA). METHODS: In this pilot study of 7 patients with BEB, we experimentally reduced cortical excitability of 4 areas: MC (first dorsal interosseus area), PMC, SMA, and AC, each with 3 noninvasive techniques: low-frequency repetitive transcranial magnetic stimulation (lfrTMS), continuous theta burst stimulation (cTBS), and cathodal transcranial direct current stimulation (tDCS). Primary outcome was the clinical effects on blepharospasm (blink rate observation by an investigator blinded to the intervention and subjective rating by the patient); secondary outcome was the blink reflex recovery curve (BRR). RESULTS:lfrTMS resulted in a significant improvement over all 4 brain areas for physician rating, patient rating, and BRR, whereas cTBS and tDCS showed only trends for improvement in physician rating, but no improvements for patient rating and BRR. lfrTMS had a significantly higher effect over AC than MC for physician rating, but no differences were seen for other pairwise comparisons of stimulated brain areas. CONCLUSIONS: Electrophysiologic and clinical improvements by functional inhibition of the medial frontal areas using low-frequency repetitive transcranial magnetic stimulation suggests that hypersensitivity of the anterior cingulate is directly or indirectly involved in the pathophysiology of benign essential blepharospasm. Inhibition of these areas using low-frequency repetitive transcranial magnetic stimulation could provide a therapeutic tool and is worthy of a larger study.
RCT Entities:
BACKGROUND: Traditionally, benign essential blepharospasm (BEB) is considered a disorder caused by basal ganglia dysfunction. Electrophysiologic and brain imaging studies suggest pathologic changes in excitability in the primary motor cortex (MC), anterior cingulate (AC), and secondary motor areas, such as premotor (PMC) and supplementary motor cortices (SMA). METHODS: In this pilot study of 7 patients with BEB, we experimentally reduced cortical excitability of 4 areas: MC (first dorsal interosseus area), PMC, SMA, and AC, each with 3 noninvasive techniques: low-frequency repetitive transcranial magnetic stimulation (lfrTMS), continuous theta burst stimulation (cTBS), and cathodal transcranial direct current stimulation (tDCS). Primary outcome was the clinical effects on blepharospasm (blink rate observation by an investigator blinded to the intervention and subjective rating by the patient); secondary outcome was the blink reflex recovery curve (BRR). RESULTS: lfrTMS resulted in a significant improvement over all 4 brain areas for physician rating, patient rating, and BRR, whereas cTBS and tDCS showed only trends for improvement in physician rating, but no improvements for patient rating and BRR. lfrTMS had a significantly higher effect over AC than MC for physician rating, but no differences were seen for other pairwise comparisons of stimulated brain areas. CONCLUSIONS: Electrophysiologic and clinical improvements by functional inhibition of the medial frontal areas using low-frequency repetitive transcranial magnetic stimulation suggests that hypersensitivity of the anterior cingulate is directly or indirectly involved in the pathophysiology of benign essential blepharospasm. Inhibition of these areas using low-frequency repetitive transcranial magnetic stimulation could provide a therapeutic tool and is worthy of a larger study.
Authors: Y H Sohn; B Voller; M Dimyan; A St Clair Gibson; T Hanakawa; F E Leon-Sarmiento; H Y Jung; M Hallett Journal: Clin Neurophysiol Date: 2004-02 Impact factor: 3.708
Authors: M Cincotta; A Borgheresi; C Gambetti; F Balestrieri; L Rossi; G Zaccara; M Ulivelli; S Rossi; C Civardi; R Cantello Journal: Clin Neurophysiol Date: 2003-10 Impact factor: 3.708
Authors: M Aramideh; J L Eekhof; L J Bour; J H Koelman; J D Speelman; B W Ongerboer de Visser Journal: J Neurol Neurosurg Psychiatry Date: 1995-06 Impact factor: 10.154
Authors: David A Peterson; Gwen C Littlewort; Marian S Bartlett; Antonella Macerollo; Joel S Perlmutter; H A Jinnah; Mark Hallett; Terrence J Sejnowski Journal: Neurology Date: 2016-10-21 Impact factor: 9.910
Authors: P Schwingenschuh; P Katschnig; M J Edwards; J T H Teo; L V P Korlipara; J C Rothwell; K P Bhatia Journal: Neurology Date: 2011-02-15 Impact factor: 9.910
Authors: Silvina G Horovitz; Anastasia Ford; Muslimah Ali Najee-Ullah; John L Ostuni; Mark Hallett Journal: Transl Neurodegener Date: 2012-06-15 Impact factor: 8.014