Year: 2011
Type: book-chapter
Abstract: IntroductionParkinson's disease is one of the most common movement disorders characterized by bradykinesia, rigidity, resting tremor and postural instability (Fahn, 2003).It affects nearly five million elderly people worldwide (de Lau & Breteler, 2006).As the population ages, the incidence and prevalence of Parkinson's disease are expected to increase dramatically (Dorsey et al., 2007;Tanner & Goldman, 1996;Tanner & Ben-Shlomo, 1999).Rigidity is one of the clinical hallmark symptoms that characterize and define Parkinson's disease.Rigidity is one form of the increased muscle tone, which is defined as a resistance to a passive movement.Rigidity is clinically characterized by an increase in muscle tone, and is felt as a constant and uniform resistance to the passive movement of a limb persisting throughout its range (Bantam, 2000;Fung & Thompson, 2002;Hallett, 2003).There are two types of rigidity: plastic or lead-pipe rigidity, in which resistance remains uniform, constant and smooth, such as experienced when bending a piece of lead; and cogwheel rigidity, in which tremor is superimposed on increased tone, giving rise to the perception of intermittent fluctuation in muscle tone.The latter is principally attributable to the combination of plastic rigidity and tremor.In addition to being a key element of parkinsonian rigidity, increased muscle tone also characterizes spasticity which is a common motor symptom in a few other neurological disorders, such as multiple sclerosis, stroke and cerebral palsy.Spasticity is clinically described as an increased resistance to passive movement due to hyperexcitability of stretch reflex (Lance, 1980;Rymer & Katz, 1994).Rigidity and spasticity share the characteristic feature of the increased muscle tone to a passive movement.However, the unique lead-pipe resistance can distinguish the increased muscle tone in rigidity from that associated with spasticity.In particular, the differentiation between rigidity and spasticity is not straightforward in a clinical scenario (Fung & Thompson, 2002).Rigidity generally responds well to dopaminergic medication and surgical intervention.Thus, it is used as a diagnostic criterion and to evaluate the efficacy of therapeutic interventions (Prochazka et al., 1997).Clinical examination and assessment of rigidity is determined by an examiner's perception of resistance while rotating the limb at major joints, based upon the Unified Parkinson Disease Rating Scale (Fahn & Elton, 1987;Goetz et al., 2008).A better understanding of the physiological and biomechanical characteristics of rigidity merits scientific significance and clinical implication.In this chapter, studies on www.intechopen.comEtiology and Pathophysiology of Parkinson's Disease 486 elucidation of the physiological mechanisms and biomechanical quantification of parkinsonian rigidity will be reviewed and the latest research on this topic will be presented. Physiological studies of parkinsonian rigidity Reflex responses to passive stretchThe 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, www.intechopen.com
Source: InTech eBooks
DOI: 10.5772/17849
Author: Ruiping Xia
Institution: Creighton University
Language: English
Subfield: Clinical Neurology
Field: Medicine
Domain: Health Sciences
Open Access status: hybrid
OpenAlex ID: W1482235397