Monoaminergic Inhibitory Control of Spinal Interneurons

Abstract

Several observations indicate that a failing monoaminergic control of spinal interneurons may be one of the main causes of the exaggerated stretch, flexion, and postural reflexes associated with spasticity: (a) The exaggerated stretch reflex may involve responses evoked by group II as well as by group muscle spindle afferents (e.g., Burke et al. 1970, 1972; Ashby and McCrea 1987; Burke 1985). (b) Responses of group II origin are to a much greater extent evoked via interneurons than by direct actions of group II muscle afferents upon motoneurons (see Lundberg et al. 1977). (c) Interneurons interposed between group II muscle afferents and motoneurons (referred to as “group II interneurons”) may mediate stretch-evoked excitation of motoneurons as well as flexion reflexes, crossed extension reflexes, and labyrinthine and neck reflexes, because sensory fibers and neurons that induce these reflexes utilize to a great extent the same interneurons (for references see Jankowska and Edgley 1993; Jankowska 1992). When group interneurons become hyperexcitable they thus may be responsible for exaggeration of not only stretch, but also flexion and postural reflexes, (d) Two of the drugs that depress transmission from group II muscle spindle afferents (Edgley et al. 1988; Bras et al. 1989, 1990), skin receptors (Barbeau et al. 1987), and nociceptors (e.g., Belcher et al. 1978; Headley et al. 1978; Davies and Johnston 1984; Fleetwood-Walker et al. 1985) also reduce muscle tonus and exaggerated stretch and flexion reflexes in spastic patients.