Hypokinetic laryngeal movement disorders are observed most often in individuals diagnosed with the neurological disorder, parkinsonism. Parkinsonism has the following features: bradykinesia, postural instability, rigidity, resting tremor, and freezing (motor blocks) (Fahn, 1986). For the diagnosis to be made, at least two of these five features should be present, and one of the two features should be either tremor or rigidity. Parkinsonism as a syndrome can be classified as idiopathic Parkinson's disease (PD) (i.e., symptoms of unknown cause); secondary (or symptomatic) PD, caused by a known and identifiable cause; or parkinsonism-plus syndromes, in which symptoms of parkinsonism are caused by a known gene defect or have a distinctive pathology. The specific diagnosis depends on findings in the clinical history, the neurological examination, and laboratory tests. No single feature is completely reliable for differentiating among the different causes of parkinsonism.

Idiopathic PD is the most common type of parkinsonism encountered by the neurologist. Pathologically, idiopathic PD affects many structures in the central nervous system (CNS), with preferential involvement of dopaminergic neurons in the substantia nigra pars compacta (SNpc). Lewy bodies, eosinophilic intracytoplasmatic inclusions, can be found in these neurons (Galvin, Lee, and Trojanowski, 2001). Alpha-synuclein is the primary component of Lewy body fibrils (Galvin, Lee, and Trojanowski, 2001). However, only about 75% of patients with the clinical diagnosis of idiopathic PD are found at autopsy to have the pathological CNS changes characteristic of PD (Hughes et al., 1992).

Many patients and their families consider the reduced ability to communicate one of the most difficult aspects of PD. Hypokinetic dysarthria, characterized by a soft voice, monotone, a breathy, hoarse voice quality, and imprecise articulation (Darley, Aronson, and Brown, 1975; Logemann et al., 1978), and reduced facial expression (masked facies) contribute to limitations in communication in the vast majority of individuals with idiopathic PD (Pitcairn et al., 1990). During the course of the disease, approximately 45%–89% of patients will report speech problems (Logemann and Fisher, 1981; Sapir et al., 2002). Repetitive speech phenomena (Benke et al., 2000), voice tremor, and hyperkinetic dysarthria may also be encountered in individuals with idiopathic PD. When hyperkinetic dysarthria is reported in idiopathic PD, it is most frequently seen together with other motor complications (e.g., dyskinesia) of prolonged levodopa therapy (Critchley, 1981).

Logemann et al. (1978) suggested that the clusters of speech symptoms they observed in 200 individuals with PD represented a progression in dysfunction, beginning with disordered phonation in recently diagnosed patients and extending to include disordered articulation and other aspects of speech in more advanced cases. Recent findings by Sapir et al. (2002) are consistent with this suggestion. Sapir et al. (2002) observed voice disorders in individuals with recent onset of PD and low Unified Parkinson Disease Rating Scale (UPDRS) scores; in individuals with longer duration of disease and higher UPDRS scores, they observed a significantly higher incidence of abnormal articulation and fluency, in addition to the disordered voice. Hypokinetic dysarthria of parkinsonism is considered to be a part of basal ganglia damage (Darley, Aronson, and Brown, 1975). However, there are no studies on pathological changes in the hypokinetic dysarthria of idiopathic PD. A significant correlation between neuronal loss and gliosis in SNpc and substantia nigra pars reticulata (SNpr) and severity of hypokinetic dysarthria was found in patients with Parkinson-plus syndromes (Kluin et al., 2001). Speech and voice characteristics may differ between idiopathic PD and Parkinson-plus syndromes (e.g., Shy-Drager syndrome, progressive supranuclear palsy, multisystem atrophy). In addition to the classic hypokinetic symptoms, these patients may have more slurring, a strained, strangled voice, pallilalia, and hypernasality (Countryman, Ramig, and Pawlas, 1994) and their symptoms may progress more rapidly.

Certain aspects of hypokinetic dysarthria in idiopathic PD have been studied extensively. Hypophonia (reduced loudness, monotone, a breathy, hoarse quality) may be observed in as many as 89% of individuals with idiopathic PD (Logemann et al., 1978). Fox and Ramig (1997) reported that sound pressure levels in individuals with idiopathic PD were significantly lower (2–4 dB [30 cm]) across a variety of speech tasks than in an age-and sex-matched control group. Lack of vocal fold closure, including bowing of the vocal cords and anterior and posterior chinks (Hanson, Gerratt, and Ward, 1984; Smith et al., 1995), has been implicated as a cause of this hypophonia. Perez et al. (1996) used videostroboscopic observations to study vocal fold vibration in individuals with idiopathic PD. They reported abnormal phase closure and symmetry and tremor (both at rest and during phonation) in nearly 50% of patients. Whereas reduced loudness and disordered voice quality in idiopathic PD have been associated with glottal incompetence (lack of vocal fold closure—e.g., bowing; Hanson, Gerratt, and Ward, 1984; Smith et al., 1995; Perez et al., 1996), the specific origin of this glottal incompetence has not been clearly defined. Rigidity or fatigue secondary to rigidity, paralysis, reduced thyroarytenoid longitudinal tension secondary to cricothyroid rigidity (Aronson, 1990), and misperception of voice loudness (Ho, Bradshaw, and Iansek 2000; Sapir et al., 2002) are among the explanations. It has been suggested that glottal incompetence (e.g., vocal fold bowing) might be due to loss of muscle or connective tissue volume, either throughout the entire vocal fold or localized near the free margin of the vocal fold. Recent physiological studies of laryngeal function in idiopathic PD have shown a reduced amplitude of electromyographic activity in the thyroarytenoid muscle accompanying glottal incompetence when compared with both aged-matched and younger controls (Baker et al., 1998). These findings and the observation of reduced and variable single motor unit activity in the thyroarytenoid muscle of individuals with idiopathic PD (Luschei et al., 1999) are consistent with a number of hypotheses, the most plausible of which is reduced central drive to laryngeal motor neuron pools.

Although the origin of the hypophonia in PD is currently undefined, Ramig and colleagues (e.g., Fox et al., 2002) have hypothesized that there are at least three features underlying the voice disorder in individuals with PD: (1) an overall neural amplitude scaledown (Penny and Young, 1983) to the laryngeal mechanism (reduced amplitude of neural drive to the muscles of the larynx); (2) problems in sensory perception of effort (Berardelli et al., 1986), which prevents the individual with idiopathic PD from accurately monitoring his or her vocal output; which results in (3) the individual's difficulty in independently generating (through internal cueing or scaling) adequate vocal effort (Hallet and Khoshbin, 1980) to produce normal loudness. Reduced neural drive, problems in sensory perception of effort, and problems scaling adequate vocal output effort may be significant factors underlying the voice problems in individuals with PD.