Phasic Ankle Reflex in Spasticity and Parkinsonian Rigidity

Mechanism of the inverted supinator reflex. A clinical and neurophysiological study.

“…On the other hand, Landau and Clare (1964) found that electrically and mechanically induced reflexes on the spastic side were increased to the same extent, indicating both an increased sensitivity of the dynamic spindles and an increased excitability of the alpha motoneurones. More recently, Dietrichson (1971) was able to prove, using mechanically and electrically induced reflexes, that both mechanisms are very clearly operating. The absence of a direct finger flexor myotatic response at a time when finger flexion could be elicited by a blow on the styloid process is evidence against stimulation of the spindles of the finger flexor group.…”

“…This has been postulated to be the stimulation of spindles of the muscles involved due to heightened sensitivity of the spindles (Lance, 1965;Lance and de Gail, 1965). An alternative explanation, proposed by several authors (Dietrichson, 1971;Landau and Clare, 1964), is that an increase in alpha motoneurone excitability exists in spasticity, and this may also explain this phenomenon. Recently, Dietrichson showed that the hyperactive ankle jerk of spastic subjects is due to both hypersensitivity of the spindles and an increase in alpha motoneurone excitability (Dietrichson, 1971).…”

“…An alternative explanation, proposed by several authors (Dietrichson, 1971;Landau and Clare, 1964), is that an increase in alpha motoneurone excitability exists in spasticity, and this may also explain this phenomenon. Recently, Dietrichson showed that the hyperactive ankle jerk of spastic subjects is due to both hypersensitivity of the spindles and an increase in alpha motoneurone excitability (Dietrichson, 1971). In the light of the 'peripheral' hypothesis the contraction of the finger flexors will be due to stimulation of the spindles of the finger flexor muscles, given to the positive bias of the gamma system of these muscles.…”

Physiological and Biomechanical Analyses of Rigidity in Parkinson's Disease

“…Recent studies using electrophysiological techniques demonstrated that monosynaptic segmental stretch reflexes showed no significant differences between individuals with Parkinson's disease and healthy controls (Bergui et al, 1992;Delwaide, 1985;Delwaide et al, 1986;Meara and Cody, 1993;Rothwell et al, 1983). Numerous studies on stretch reflexes have also shown that most reflexes (H-reflex, tendon jerks and tonic vibration reflex), considered to be principally mediated by Ia afferents and to be spinal in origin, appear normal in Parkinson's disease (Burke et al, 1972a;Dietrichson, 1971;Lance et al, 1973). In brief, there is no evidence that Ia muscle afferent pathway might explain the pathophysiological basis of parkinsonian rigidity.…”

“…However, it is certain that patients with parkinsonian rigidity show a marked increase in long-latency stretch reflexes, compared with healthy controls (Marsden, 1990;Fung & Thompson, 2002), though there is no universal agreement as to the origin of the longlatency stretch reflexes (Matthews, 1991). In addition, the tonic muscle response to slow and sustained stretch is reported to be exaggerated in Parkinson's disease (Dietrichson, 1971;Andrews et al, 1972). Findings obtained from the aforementioned studies provide partial explanations for increased resistance, i.e., one of the two elements defining parkinsonian rigidity.…”