Motor neuron ‘bistability’: A pathogenetic mechanism for cramps and myokymia

Abstract

In three patients suffering from chronic muscle cramps, spasms and myokymia, these involuntary contractions were triggered in the triceps surae, quadriceps, flexor carpi radialis or flexor digitorum by means of single or short-train stimulation of homonymous Ia afferents, elicited by electrical means or tendon taps. In some cases cramp was induced by the first afferent volleys; more often, however, continued stimulation produced stepwise recruitment of motor units (whose rhythmic firing was visible as myokymia in the muscle) until cramp developed. Cramps and myokymic discharges could usually be terminated by a single maximal stimulus to the motor axons (producing antidromic invasion and Renshaw inhibition of the motor neurons), or by short trains of volleys in inhibitory pathways from the skin. The fact that it was possible to induce myokymia and cramps by brief synaptic excitation and terminate them by antidromic invasion or synaptic inhibition, suggests that the mechanism generating these disturbances is intrinsic to alpha-motor neuron somata. Similar on-off switching of self-sustained motor discharges has been observed in the decerebrate cat and is known to depend on 'bistability' of the motor neuron membrane. We propose that a similar mechanism is responsible for discharges that produce cramp.

Large Involuntary Forces Consistent with Plateau-Like Behavior of Human Motoneurons

“…Similarly, because the stimulation activates a portion of the muscle not normally activated by direct motor axon stimulation, it may have applications in reducing the muscle atrophy resulting from disuse associated with acute or chronic injury conditions. Plateau potentials have been invoked in other studies on human subjects to explain cramp-like behavior (Baldissera et al, 1991(Baldissera et al, , 1994, self-sustained discharges (Kiehn and Eken, 1997;Gorassini et al, 1998), and the potential discrepancy between the forces at recruitment and derecruitment of motor units (Heckman and Lee, 1999). Whereas these studies focused on EMG recordings and the properties of single motor units, our study focused on the resulting forces and suggests that these intrinsic mechanisms can generate large forces and thereby make a substantial contribution to the control of voluntary movement.…”

Imbalance of ionic conductances contributes to diverse symptoms of demyelination

“…Regulating g L could control axon excitability (synergistically with g Na ) in the course of demyelination and its sequalae (21,22). Although AD and bistability have been described in more complex systems (23,24), and other factors including impedance mismatch (itself related to local input resistance) contribute to excitability in a spatially extended model (25), our model demonstrates the sufficiency of g Na /g L (in the presence of g Nap ) to explain four excitability states that may underlie the positive and negative symptoms of demyelination. Furthermore, given that qualitative excitability changes can result from small changes in α, the intermittence of symptoms may reflect operation of the axon near one of its critical transition boundaries.…”

Metabotropic Modulation of Motoneurons by Scratch-Like Spinal Network Activity

“…Despite being studied intensely, their function and significance remain controversial and unsettled. Some studies emphasize a possible involvement in pathology such as spinal seizures (Kao and Crill, 1972;Davenport et al, 1977) cramps (Baldissera et al, 1991(Baldissera et al, , 1994, and spasticity (Bennett et al, 2001a,b). In normal function PIC has been considered a mechanism for secondary range firing (Crill and Schwindt, 1984), bistability (Hounsgaard et al, 1984, gain control (Hounsgaard et al, 1986), boost of synaptic excitation (Lee and Heckman, 2000), and regulation of recruitment order (Delgado-Lezama et al, 1997).…”