لکنت زبان و مدارهای گانگلیون بازال: نقد و ارتباط احتمالی
|کد مقاله||سال انتشار||مقاله انگلیسی||ترجمه فارسی||تعداد کلمات|
|33487||2004||45 صفحه PDF||سفارش دهید||22966 کلمه|
Publisher : Elsevier - Science Direct (الزویر - ساینس دایرکت)
Journal : Journal of Communication Disorders, Volume 37, Issue 4, July–August 2004, Pages 325–369
The possible relation between stuttering and the basal ganglia is discussed. Important clues to the pathophysiology of stuttering are given by conditions known to alleviate dysfluency, like the rhythm effect, chorus speech, and singing. Information regarding pharmacologic trials, lesion studies, brain imaging, genetics, and developmental changes of the nervous system is reviewed. The symptoms of stuttering are compared with basal ganglia motor disorders like Parkinson’s disease and dystonia. It is proposed that the basal ganglia-thalamocortical motor circuits through the putamen are likely to play a key role in stuttering. The core dysfunction in stuttering is suggested to be impaired ability of the basal ganglia to produce timing cues for the initiation of the next motor segment in speech. Similarities between stuttering and dystonia are indicated, and possible relations to the dopamine system are discussed, as well as the interaction between the cerebral cortex and the basal ganglia. Behavioral and pharmacologic information suggests the existence of subtypes of stuttering.
Research concerning the nature of stuttering has produced an extensive amount of data during the past century, but the mechanisms behind the speech disruptions and the speech initiation problems are still not clear. An intriguing aspect of stuttering is the various conditions which can temporarily alleviate dysfluency in most cases: the rhythm effect (speaking to the pace of a metronome), singing, chorus speech, and altered auditory feedback (Wingate, 2002). The often dramatic improvements in fluency caused by these conditions indicate that stuttering is not the result of some general speech motor instability, instead there seem to be specific causal mechanisms leading to the speech problems. In this article, possible relationships between stuttering and the functions of the basal ganglia (BG) circuits are reviewed and discussed. This review leads to the proposal that the circuits through the basal ganglia play a key role in the mechanisms of stuttering. The BG are the largest subcortical structures in the human forebrain, and they are placed in a key position to influence motor behavior, emotions, and cognition (Graybiel, 2000). The idea that stuttering may be related to the BG is not new. As early as 1934, Seeman suggested that stuttering is the result of disturbed BG function (as cited in Van Riper, 1982). More recent suggestions for BG involvement in stuttering come from Rosenberger (1980), Caruso (1991), Wu et al. (1995), Lebrun (1998), and Victor and Ropper (2001), and others. First an overview of the basal ganglia anatomy and functions will be presented. Thereafter several aspects of basal ganglia functions and disorders will be discussed in relation to stuttering: motor control and timing, lesions, brain imaging, dopamine, emotional influences, developmental changes of the BG, and similarities between stuttering and disorders like Parkinson’s disease and dystonia. The BG operate in a close relation with the cerebral cortex, and therefore some important findings about the cortex and stuttering will also be discussed, from the perspective of the basal ganglia functions. Lastly tentative conclusions will be presented. Among the suggested conclusions can be mentioned that the core dysfunction in stuttering is proposed to be impaired ability of the basal ganglia to produce timing cues, that developmental changes of dopamine receptor density in the putamen might explain the frequent pattern of early childhood onset and recovery of stuttering, and that stuttering is likely to be a heterogeneous disorder with subtypes showing different responses to different types of dopaminergic medication. 2. Overview of the basal ganglia anatomy and functions Even though the understanding of the BG circuits still must be considered as highly incomplete, knowledge has grown rapidly during the last decades. The model presented here is simplified, mainly limited to the aspects most relevant to the discussion. (For more thorough reviews, see for example Mink, 1996, and Victor & Ropper, 2001.) The basal ganglia consist of a set of interconnected subcortical nuclei. The main input nucleus is the striatum, which receives topographical excitatory projections from almost the entire cerebral cortex, especially from the sensorimotor and frontal cortex ( Parent, 1996). The striatum and the downstream structures in the basal ganglia are organized in topographically and functionally segregated pathways. The cortical inputs to the striatum are convergent, for example in such a way that sensory and motor cortex areas converge into single striatal zones ( Flaherty & Graybiel, 1991). The striatum is located close to the globus pallidus, which is divided into an external (GPe) and an internal part (GPi) ( DeLong, 2000). The GPi is one of the main output nuclei 1 of the BG, and it projects, via various nuclei in the thalamus, to most cortical areas of the frontal lobe ( Alexander, Crutcher, & DeLong, 1990). This architecture means that the BG is part of extensive loops, basal ganglia-thalamocortical circuits, which link almost the entire cortex to the cortex of the frontal lobe. The GPi also has descending output to the brain stem. Through this pathway the BG can influence brain stem functions like inhibition of auditory input ( Swerdlow & Geyer, 1999). In summary, the BG modulate the activity of the frontal cortex and the activity of parts of the brain stem. The striatum can be divided into three main parts: (a) the putamen, (b) the caudate nucleus, and (c) the ventral striatum. This division roughly corresponds to a functional division of the basal ganglia-thalamocortical circuits: (a) (sensori)motor circuits of the putamen, with output to the primary motor cortex, the supplementary motor area (SMA), and the premotor cortex; (b) associative circuits of the caudate nucleus, with output to the prefrontal cortex; and (c) limbic circuits of the ventral striatum, with output to the anterior cingulate cortex and medial prefrontal cortex ( DeLong, 2000 and Parent, 1996). The ventral (limbic) striatum also receives input from limbic structures, such as the amygdala and hippocampus ( Joel & Weiner, 2000). The striatum projects to the GPi by two pathways, the direct and the indirect (see Fig. 1). The indirect pathway also includes the subthalamic nucleus (STN). All projections from the striatum, the GPe, and the GPi are inhibitory, while the projections from the cortex, the STN and the thalamus are excitatory. The GPi is tonically active, thereby suppressing thalamic activity. Activation of the direct pathway inhibits neurons in the GPi, which in turn disinhibits thalamic neurons, finally resulting in excitation of cortical neurons. Activation of the indirect pathway has the opposite effect, activating the GPi and thereby inhibiting the cortex ( DeLong, 2000). In this way the two pathways balance each other, modulating cortical activity.
نتیجه گیری انگلیسی
The following tentative conclusions are proposed, with the intention of suggesting pathways for further research. (a) There are strong indications that the basal ganglia-thalamocortical motor circuit, through the putamen to the SMA, plays an important role in the pathophysiology of stuttering. The dysfunction may have various causes and may be the effect of interaction between several factors. Possible factors might be, for example: high density of D2-receptors and low D1/D2 ratio in the putamen; aberrant levels of dopamine release; and focal lesions of the basal ganglia-thalamocortical circuit. (b) The core dysfunction in stuttering is suggested to be impaired ability of the basal ganglia to produce timing cues. Some of the conditions that temporarily alleviate stuttering are proposed to be effective by providing compensatory timing information. This pertains to the rhythm effect, chorus speech, and singing. The adaptation effect is mainly based on an improvement of the basal ganglia timing cues resulting from practice of a specific speech sequence. (c) Other conditions that tend to alleviate stuttering are suggested to be effective because of de-automatization of the speech control. This would apply to novel modes of speaking and to masked or frequency altered auditory feedback. The effect of altered auditory feedback might also be related to attenuation of the effective feedback signal. (d) Influence of emotions and stress on stuttering is well compatible with the suggestion of stuttering as a basal ganglia disorder. (e) Concomitant symptoms, such as involuntary movements, are thought to be the result of specific mechanisms related to the basal ganglia circuits, prevalent in some but not in all cases of stuttering. (f) A morphological study suggests the importance of cerebral cortex anomalies in persistent stuttering, possibly in interaction with the basal ganglia functions. (g) The typical pattern of early childhood onset of stuttering and subsequent recovery in many cases is proposed to be related to a peak in D2-receptor density in the putamen about the age of 2–3, in combination with a relatively low D1/D2 ratio in some children, especially boys. This factor is suggested to be particularly important in stuttering children with precocious language development. (h) Stuttering is a heterogeneous disorder and characterization of subtypes is an important task for research. Based on differential traits (Daly, 1996 and Van Riper, 1982), and differential responses to medication (Langova & Moravek, 1964) two preliminary subtypes are suggested (it should be noticed that the proposed differential pharmacologic effects are based on very few cases): Stuttering type 1: This group corresponds to what Daly (1996) defined as “stuttering” (as opposed to “stuttering-cluttering”) and is similar to Van Riper’s tracks I and III ( Van Riper, 1982), and may constitute the majority of persons who stutter. There are some indications that the speech in this subgroup tends to improve on dopamine stimulants and to get worse on D2-blockers (it is too early, however, to draw any conclusions about dopamine stimulants in the treatment of stuttering). The onset of stuttering occurs after a period of fluent speech, and tense speech initiation blocks often become an important part of the problem. The stuttering tends to get worse in relation to negative emotional reactions. Stuttering type 2: This group corresponds to what has been called “stuttering-cluttering” ( Daly, 1996) and is similar to Van Riper’s track II ( Van Riper, 1982). There are indications that the stuttering tends to improve on D2-blockers and to get worse on dopamine stimulants. Frequent behavioral traits may be increased behavioral activation, high speech rate, and talkativeness.