**2. Physiological studies of parkinsonian rigidity**

#### **2.1 Reflex responses to passive stretch**

The history of studying the pathophysiology of rigidity can be traced back to nearly a century ago. Forester's observation (1921) that parkinsonian rigidity is reduced by the dorsal root section suggested that rigidity could be of reflex origin, although other equally plausible explanations are possible. The most widespread view was that rigidity arose from the increased response of muscle receptors to externally imposed stretch. This view was supported by earlier experiments (Pollock & Davis, 1930; Rushworth, 1960), demonstrating that rigidity was substantially reduced by dorsal root section or local anesthetic block.

However, illustration by microneurographic recordings from muscle nerves has provided evidence that increased muscle afferent discharge (due to increased fusimotor drive) was not sufficient to explain the presence of rigidity (Burke et al., 1977). 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.

If the response of the spinal machinery to muscle primary spindle afferent input is intact in Parkinson's disease, supraspinally mediated reflexes might well play a role in the pathophysiology of rigidity. Lee and Tatton (1975) were the first to demonstrate that longlatency stretch reflexes in forearm muscles were exaggerated in patients with Parkinson's disease. This observation was subsequently confirmed by several other investigators who studied rigidity in the same or different muscle groups (Berardelli et al., 1983; Cody et al., 1986; Mortimer & Webster, 1979; Rothwell et al., 1983). Some studies found a quantitative association between the degree of increase in long-latency stretch reflex and the clinically assessed degree of rigidity (Mortimer & Webster, 1979; Berardelli et al., 1983), whereas others found that no correlation existed between the two based on a larger number of patients (Cody et al., 1986; Rothwell et al., 1983). The lack of a consistent correlation might be because rigidity is often assessed using a sustained static stretch whereas long-latency stretch reflexes is elicited by transient and brisk muscle stretches (Marsden, 1990). 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. However,

elucidation of the physiological mechanisms and biomechanical quantification of parkinsonian rigidity will be reviewed and the latest research on this topic will be

The history of studying the pathophysiology of rigidity can be traced back to nearly a century ago. Forester's observation (1921) that parkinsonian rigidity is reduced by the dorsal root section suggested that rigidity could be of reflex origin, although other equally plausible explanations are possible. The most widespread view was that rigidity arose from the increased response of muscle receptors to externally imposed stretch. This view was supported by earlier experiments (Pollock & Davis, 1930; Rushworth, 1960), demonstrating that rigidity was substantially reduced by dorsal root section or local anesthetic block. However, illustration by microneurographic recordings from muscle nerves has provided evidence that increased muscle afferent discharge (due to increased fusimotor drive) was not sufficient to explain the presence of rigidity (Burke et al., 1977). 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

If the response of the spinal machinery to muscle primary spindle afferent input is intact in Parkinson's disease, supraspinally mediated reflexes might well play a role in the pathophysiology of rigidity. Lee and Tatton (1975) were the first to demonstrate that longlatency stretch reflexes in forearm muscles were exaggerated in patients with Parkinson's disease. This observation was subsequently confirmed by several other investigators who studied rigidity in the same or different muscle groups (Berardelli et al., 1983; Cody et al., 1986; Mortimer & Webster, 1979; Rothwell et al., 1983). Some studies found a quantitative association between the degree of increase in long-latency stretch reflex and the clinically assessed degree of rigidity (Mortimer & Webster, 1979; Berardelli et al., 1983), whereas others found that no correlation existed between the two based on a larger number of patients (Cody et al., 1986; Rothwell et al., 1983). The lack of a consistent correlation might be because rigidity is often assessed using a sustained static stretch whereas long-latency stretch reflexes is elicited by transient and brisk muscle stretches (Marsden, 1990). 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,

Findings obtained from the aforementioned studies provide partial explanations for increased resistance, *i.e.*, one of the two elements defining parkinsonian rigidity. However,

**2. Physiological studies of parkinsonian rigidity** 

**2.1 Reflex responses to passive stretch** 

presented.

rigidity.

1971; Andrews et al., 1972).

they cannot account for the constancy and uniformity of resistance which is uniquely associated with rigidity. Recent studies have shed light on the underlying mechanism of the uniform nature of parkinsonian rigidity (Xia & Rymer, 2004; Xia et al., 2011). Evidence indicates that shortening reaction and stretch-induced inhibition play pivotal roles in the genesis of lead-pipe characteristics of rigidity.
