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NEUROLOGY 2006;67:52-56
© 2006 American Academy of Neurology

Lack of modulation of Ib inhibition during antagonist contraction in spasticity

H. Morita, MD, PhD, M. Shindo, MD, PhD, H. Momoi, MD, PhD, S. Yanagawa, MD, PhD, S. Ikeda, MD, PhD and N. Yanagisawa, MD, PhD

From the Department of Medicine, Shinshu University School of Medicine, Japan. Present addresses: Nagano National Hospital (M.S.), Ueda; Iida Municipal Hospital (H. Momoi, S.Y.); and Kanto Rosai Hospital (N.Y.), Nakahara, Kawasaki, Japan.

Address correspondence and reprint requests to Dr. Hiroshi Morita, Department of Medicine (Neurology), Clinical Neurophysiology Laboratory, Shinshu University School of Medicine, Asahi 3-1-1, Matsumoto, 3908621 Japan; e-mail: hmorita{at}hsp.md.shinshu-u.ac.jp

Objective: To examine the modulation of non-reciprocal group I (Ib) inhibition during tonic contraction of antagonist muscles in patients with spasticity vs normal subjects.

Methods: The authors studied 10 patients with spastic paraplegia due to cervical compression myelopathy and 16 age-matched normal subjects. Ib inhibition to soleus motoneurons was recorded as the change in size of the H-reflex of the soleus, evoked by conditioning stimulus to the nerve innervating the medial gastrocnemius muscle. The extent of inhibition was studied at rest and during tonic contraction of the pretibial muscles of variable strength.

Results: In the resting state, the extent of inhibition in the patients did not differ from normal controls. During antagonist contraction, the extent of inhibition increased both in the normal subjects and patients. The increment was smaller in the patients, especially in those with severe spastic gait. The smaller increment in the inhibition was correlated with the time required to walk 10 m in the patients.

Conclusion: The authors observed a lack of modulation of Ib inhibition during tonic antagonist contraction in patients with spasticity, especially those with gait disturbance. Disturbed central modulation of non-reciprocal (Ib) interneurons may be responsible for spasticity.

Supported by a Grant-in-Aid for Scientific Research from the Ministry of Education, Science, and Culture of Japan (No. 03670417, 11770327, 14570584, 16590820).

Disclosure: The authors report no conflicts of interest.

Received August 23, 2005.

Accepted in final form March 20, 2006.






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