Relationship between muscle spindles and myofascial trigger spots according to Hoffmann reflex pathway and tissue morphology characteristics in a rat model.

OBJECTIVES: To determine how muscle spindles are involved in the pathophysiology of chronic myofascial trigger spots (MTrSs, similar to myofascial trigger points) in a rat injury model according to the characteristics of the Hoffmann reflex (H-reflex) and the anatomical relationship between muscle spindles and MTrSs. METHODS: 16 male Sprague-Dawley rats (7 weeks old) were randomly divided into experimental and control groups. A blunt strike injury and eccentric exercise were applied to the gastrocnemius muscle of rats in the experimental group once a week for 8 weeks as a MTrS modelling intervention. Subsequently, the rats were reared normally and rested for 4 weeks. At the end of the 12th week, the rats were examined for the presence of MTrSs defined by the detection of a palpable taut band exhibiting both a local twitch response and spontaneous electrical activity. After modelling, evocation of the H-reflex and morphological examination of muscle spindles and MTrSs were conducted. RESULTS: The threshold (0.35±0.04 mA) of the H-reflex and latency (1.24±0.18 ms) of the M wave recorded at MTrSs were not significantly different to those at non-MTrSs (P>0.05). Compared with non-MTrSs, a lower Mmax (4.28±1.27 mV), higher Hmax (median (IQR) 0.95 (0.80-1.08) mV) and Hmax/Mmax (median (IQR) 0.21 (0.16-0.40)), and shorter H wave latency (4.60±0.89 ms) were recorded at MTrSs (P<0.05). Morphologically, there was a close anatomical relationship between the MTrS cells and the muscle spindles. DISCUSSION: Compared with normal muscles, the H-reflex myoelectrical activity was enhanced and some muscle spindles might have been influenced by active MTrSs. Thus, muscle spindles may play an important role in the pathological mechanism underlying myofascial trigger points.

The effects of experimental muscle and skin pain on the static stretch sensitivity of human muscle spindles in relaxed leg muscles.

Animal studies have shown that noxious inputs onto gamma-motoneurons can cause an increase in the activity of muscle spindles, and it has been proposed that this causes a fusimotor-driven increase in muscle stiffness that is believed to underlie many chronic pain syndromes. To test whether experimental pain also acts on the fusimotor system in humans, unitary recordings were made from 19 spindle afferents (12 Ia, 7 II) located in the ankle and toe extensors or peronei muscles of awake human subjects. Muscle pain was induced by bolus intramuscular injection of 0.5 ml 5% hypertonic saline into tibialis anterior (TA); skin pain was induced by 0.2 ml injection into the overlying skin. Changes in fusimotor drive to the muscle spindles were inferred from changes in the mean discharge frequency and discharge variability of spindle endings in relaxed muscle. During muscle pain no afferents increased their discharge activity: seven afferents (5 Ia, 2 II) showed a decrease and six (4 Ia, 2 II) afferents were not affected. During skin pain of 13 afferents discharge rate increased in one (Ia) and decreased in two (1 Ia, 1 II). On average, the overall discharge rate decreased during muscle pain by 6.1% (P < 0.05; Wilcoxon), but remained essentially the same during skin pain. There was no detectable correlation between subjective pain level and the small change in discharge rate of muscle spindles. Irrespective of the type of pain, discharge variability parameters were not influenced (P > 0.05; Wilcoxon). We conclude that, contrary to the 'vicious cycle' hypothesis, acute activation of muscle or skin nociceptors does not cause a reflex increase in fusimotor drive in humans. Rather, our results are more aligned with the pain adaptation model, based on clinical studies predicting pain-induced reductions of agonist muscle activity.

Experimental muscle pain produces central modulation of proprioceptive signals arising from jaw muscle spindles.

The aim of the present study was to investigate the effects of intramuscular injection with hypertonic saline, a well-established experimental model for muscle pain, on central processing of proprioceptive input from jaw muscle spindle afferents. Fifty-seven cells were recorded from the medial edge of the subnucleus interpolaris (Vi) and the adjacent parvicellular reticular formation from 11 adult cats. These cells were characterized as central units receiving jaw muscle spindle input based on their responses to electrical stimulation of the masseter nerve, muscle palpation and jaw stretch. Forty-five cells, which were successfully tested with 5% hypertonic saline, were categorized as either dynamic-static (DS) (n=25) or static (S) (n=20) neurons based on their responses to different speeds and amplitudes of jaw movement. Seventy-six percent of the cells tested with an ipsilateral injection of hypertonic saline showed a significant modulation of mean firing rates (MFRs) during opening and/or holding phases. The most remarkable saline-induced change was a significant reduction of MFR during the hold phase in S units (100%, 18/18 modulated). Sixty-nine percent of the DS units (11/16 modulated) also showed significant changes in MFRs limited to the hold phase. However, in the DS neurons, the MFRs increased in seven units and decreased in four units. Finally, five DS neurons showed significant changes of MFRs during both opening and holding phases. Injections of isotonic saline into the ipsilateral masseter muscle had little effect, but hypertonic saline injections made into the contralateral masseter muscle produced similar results to ipsilateral injections with hypertonic saline. These results unequivocally demonstrate that intramuscular injection with an algesic substance, sufficient to produce muscle pain, produces significant changes in the proprioceptive properties of the jaw movement-related neurons. Potential mechanisms involved in saline-induced changes in the proprioceptive signals and functional implications of the changes are discussed.

Muscle spindle activity in the affected upper limb after a unilateral stroke.

Weakness, loss of dexterity and exaggerated reflex responses to proprioceptive and cutaneous stimuli are typical features of hemiparetic stroke. Since the extent to which altered fusimotor drive contributes to these deficits has not been established, this study was designed to assess fusimotor function in stroke patients by comparing three aspects of muscle spindle afferent behaviour (background discharge rate, responses to reflex inputs and responses to voluntary contractions) in 11 subjects affected by recent cerebrovascular lesions, with those in 18 healthy volunteers. The mean background discharge rates of muscle spindle afferents in the radial nerve when subjects attempted to relax the recorded limb completely were 6.6 +/- 5.3 Hz (n = 26) in patients and 6.4 +/- 6.1 Hz (n = 76) in control subjects. The variability of discharge rate of active afferents was also similar (0.12 +/- 0.07 and 0.09 +/- 0. 10, respectively). Reflex activation of fusimotor neurons was assessed using trains of electrical stimuli to the superficial radial nerve or to the palm of the hand, and using natural skin stimuli. Neither type of cutaneous stimulation affected muscle spindle afferent discharge in the absence of an EMG response. During deliberate voluntary contractions muscle spindle discharge rates were enhanced similarly in both the control and patient groups, indicating that volitional drives could access fusimotor neurons in the patients. Qualitatively, spindle behaviour was similar in patients and control subjects. These findings suggest that fusimotor function is not disturbed any more or less than skeletomotor function in hemiparetic patients and it is concluded that fusimotor dysfunction probably contributes little to their deficit.

Thalamo-cortical systems regulating spindle bursts and recruiting responses. II. Effect of thalamic lesions.

The effects of thalamic lesions on recruiting responses and spindle bursts have been studied in 12 cats immobilized with gallamine. Recruiting responses were elicited by stimulation of the midline thalamic nuclear complex. Spindle bursts were produced by lesions in the mesencephalic tegmentum. Recruiting responses and spindle bursts were recorded from the cortex and thalamus. The effect of thalamic lesions on such spontaneous and induced potentials was evaluated by making lesions anteriorly in the rostral pole of the thalamus, medially in the midline thalamic nuclear group, and laterally in the primary and association nuclei of the thalamus. 1. Small, anterior, thalamic lesions blocked spindle bursts and recruiting responses both at the cortex and in the thalamus. 2. Massive, medial, thalamic lesions blocked spindle bursts in the suprasylvian cortex, but did not affect either frontal cortex spindle bursts or frontal and thalamic recruiting responses induced by stimulation of N. ventralis anterior. 3. Massive, lateral, thalamic lesions including specific relay and association nuclei, failed to block spontaneous spindles and recruiting responses in frontal cortex and midline thalamic nuclei. It has been postulated that the rostral pole of the thalamus constitutes an important part of the thalamic portion of a thalamo-orbitocortical system which mediates and regulates electrocortical synchronization as manifested in spindle bursts, recruiting responses and synchronized wave-like potentials.