Volume 15, Issue 4 pp. 367-370

Intrafusal effects of botulinum toxin in post-stroke upper limb spasticity

C. Trompetto

C. Trompetto

Department of Neurosciences, Ophthalmology & Genetics, University of Genoa, Genoa, Italy

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M. Bove

M. Bove

Department of Experimental Medicine, University of Genoa, Genoa, Italy

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L. Avanzino

L. Avanzino

Department of Neurosciences, Ophthalmology & Genetics, University of Genoa, Genoa, Italy

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G. Francavilla

G. Francavilla

Department of Neurosciences, Ophthalmology & Genetics, University of Genoa, Genoa, Italy

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A. Berardelli

A. Berardelli

Department of Neurological Sciences and Neuromed Institute, University of Rome ‘La Sapienza’, Rome, Italy

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G. Abbruzzese

G. Abbruzzese

Department of Neurosciences, Ophthalmology & Genetics, University of Genoa, Genoa, Italy

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First published: 11 February 2008
Citations: 27
Prof. Giovanni Abbruzzese, Department of Neurosciences, Ophthalmology & Genetics, University of Genoa, Via De Toni 5, 16132 Genoa, Italy (tel.: +39 010 3537039; fax: +39 010 3538631; e-mail: [email protected]).

Abstract

A previous study in subjects with focal dystonia suggested that the greater and longer-lasting effect induced by botulinum toxin type A (BoNT-A) on the tonic vibration reflex (TVR) than on the maximal M-wave (M-max) might be the physiological marker of the toxin’s action at the level of intrafusal muscle fibres. With this approach, we investigated the possible effect of BoNT-A on fusimotor synapses in eight patients with post-stroke spasticity (four with no residual motor capacity before treatment and four with partially spared muscle strength and residual motor capacity). TVR and M-max were recorded from the wrist and finger flexor muscles before treatment and at 1, 4 and 7 months afterwards. The TVR reduction was greater than the M-max reduction and remained fairly constant over time only in the subjects with a residual motor capacity before the treatment. This pilot study suggests that some degree of strength and active movement is necessary for the action of BoNT-A on intrafusal fibres.

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