About: Dysarthria is a(n) research topic. Over the lifetime, 2402 publication(s) have been published within this topic receiving 56554 citation(s).
Papers published on a yearly basis
15 Jan 1995
Abstract: Part 1: Substrates 1. Defining, Understanding, and Categorizing Motor Speech Disorders 2. Neurologic Bases of Motor Speech and its Pathologies 3. Examination of Motor Speech Disorders Part 2: The Disorders and Their Diagnoses 4. Flaccid Dysarthria 5. Spastic Dysarthria 6. Ataxic Dysarthria 7. Hypokinetic Dysarthria 8. Hyperkinetic Dysarthria 9. Unilateral Upper Motor Neuron Dysarthria 10. Mixed Dysarthrias 11. Apraxia of Speech 12. Neurogenic Mutism 13. Other Neurogenic Speech Disturbances 14. Acquired Psychogenic Speech Disturbances 15. Differential Diagnosis Part 3: Management 16. Managing Motor Speech Disorders: General Principles 17. Managing the Dysarthrias 18. Managing Apraxia of Speech 19. Managing Other Neurogenic Speech Disturbances 20. Managing Acquired Psychogenic Speech Disorders
TL;DR: The cerebellar cognitive affective syndrome (CCAS) includes impairments in executive, visual-spatial, and linguistic abilities, with affective disturbance ranging from emotional blunting and depression, to disinhibition and psychotic features.
Abstract: Many diseases involve the cerebellum and produce ataxia, which is characterized by incoordination of balance, gait, extremity and eye movements, and dysarthria. Cerebellar lesions do not always manifest with ataxic motor syndromes, however. The cerebellar cognitive affective syndrome (CCAS) includes impairments in executive, visual-spatial, and linguistic abilities, with affective disturbance ranging from emotional blunting and depression, to disinhibition and psychotic features. The cognitive and psychiatric components of the CCAS, together with the ataxic motor disability of cerebellar disorders, are conceptualized within the dysmetria of thought hypothesis. This concept holds that a universal cerebellar transform facilitates automatic modulation of behavior around a homeostatic baseline, and the behavior being modulated is determined by the specificity of anatomic subcircuits, or loops, within the cerebrocerebellar system. Damage to the cerebellar component of the distributed neural circuit subserving sensorimotor, cognitive, and emotional processing disrupts the universal cerebellar transform, leading to the universal cerebellar impairment affecting the lesioned domain. The universal cerebellar impairment manifests as ataxia when the sensorimotor cerebellum is involved and as the CCAS when pathology is in the lateral hemisphere of the posterior cerebellum (involved in cognitive processing) or in the vermis (limbic cerebellum). Cognitive and emotional disorders may accompany cerebellar diseases or be their principal clinical presentation, and this has significance for the diagnosis and management of patients with cerebellar dysfunction.
TL;DR: Thirty-second speech samples were studied of at least 30 patients in each of 7 discrete neurologic groups, each patient unequivocally diagnosed as being a representative of his diagnostic group, leading to results leading to these conclusions.
Abstract: Thirty-second speech samples were studied of at least 30 patients in each of 7 discrete neurologic groups, each patient unequivocally diagnosed as being a representative of his diagnostic group. Three judges independently rated each of these samples on each of 38 dimensions of speech and voice using a 7-point scale of severity. Computer analysis based on the means of the three ratings on each patient on each dimension yielded results leading to these conclusions: (1) Speech indeed follows neuroanatomy and neurophysiology. There are multiple types or patterns of dysarthria, each mirroring a different kind of abnormality of motor functioning. (2) These patterns of dysarthria can be differentiated; they sound different. They consist of definitive groupings of certain dimensions of speech and voice, deviant to distinctive degrees. (3) Five types of dysarthria were delineated: flaccid dysarthria (in bulbar palsy), spastic dysarthria (in pseudobulbar palsy), ataxic dysarthria (in cerebellar disorders), hypokine...
TL;DR: Functional topography is considered to be a consequence of the differential arrangement of connections of the cerebellum with the spinal cord, brainstem, and cerebral hemispheres, reflecting cerebellar incorporation into the distributed neural circuits subserving movement, cognition, and emotion.
Abstract: Patients with cerebellar damage often present with the cerebellar motor syndrome of dysmetria, dysarthria and ataxia, yet cerebellar lesions can also result in the cerebellar cognitive affective syndrome (CCAS), including executive, visual spatial, and linguistic impairments, and affective dysregulation. We have hypothesized that there is topographic organization in the human cerebellum such that the anterior lobe and lobule VIII contain the representation of the sensorimotor cerebellum; lobules VI and VII of the posterior lobe comprise the cognitive cerebellum; and the posterior vermis is the anatomical substrate of the limbic cerebellum. Here we analyze anatomical, functional neuroimaging, and clinical data to test this hypothesis. We find converging lines of evidence supporting regional organization of motor, cognitive, and limbic behaviors in the cerebellum. The cerebellar motor syndrome results when lesions involve the anterior lobe and parts of lobule VI, interrupting cerebellar communication with cerebral and spinal motor systems. Cognitive impairments occur when posterior lobe lesions affect lobules VI and VII (including Crus I, Crus II, and lobule VIIB), disrupting cerebellar modulation of cognitive loops with cerebral association cortices. Neuropsychiatric disorders manifest when vermis lesions deprive cerebro-cerebellar-limbic loops of cerebellar input. We consider this functional topography to be a consequence of the differential arrangement of connections of the cerebellum with the spinal cord, brainstem, and cerebral hemispheres, reflecting cerebellar incorporation into the distributed neural circuits subserving movement, cognition, and emotion. These observations provide testable hypotheses for future investigations.
TL;DR: The ability to detect the CCAS in real time in clinical neurology with a brief and validated scale should make it possible to develop a deeper understanding of the clinical consequences of cerebellar lesions in a wide range of neurological and neuropsychiatric disorders with a link to the cerebellum.
Abstract: What the cerebellum does to sensorimotor and vestibular control, it also does to cognition, emotion, and autonomic function. This hypothesis is based on the theories of dysmetria of thought and the universal cerebellar transform, which hold that the cerebellum maintains behavior around a homeostatic baseline, automatically, without conscious awareness, informed by implicit learning, and performed according to context. Functional topography within the cerebellum facilitates the modulation of distributed networks subserving multiple different functions. The sensorimotor cerebellum is represented in the anterior lobe with a second representation in lobule VIII, and lesions of these areas lead to the cerebellar motor syndrome of ataxia, dysmetria, dysarthria and impaired oculomotor control. The cognitive / limbic cerebellum is in the cerebellar posterior lobe, with current evidence pointing to three separate topographic representations, the nature of which remain to be determined. Posterior lobe lesions result in the cerebellar cognitive affective syndrome (CCAS), the hallmark features of which include deficits in executive function, visual spatial processing, linguistic skills and regulation of affect. The affective dyscontrol manifests in autism spectrum and psychosis spectrum disorders, and disorders of emotional control, attentional control, and social skill set. This report presents an overview of the rapidly growing field of the clinical cognitive neuroscience of the cerebellum. It commences with a brief historical background, then discusses tract tracing experiments in animal models and functional imaging observations in humans that subserve the cerebellar contribution to neurological function. Structure function correlation studies following focal cerebellar lesions in adults and children permit a finer appreciation of the functional topography and nature of the cerebellar motor syndrome, cerebellar vestibular syndrome, and the third cornerstone of clinical ataxiology - the cerebellar cognitive affective syndrome. The ability to detect the CCAS in real time in clinical neurology with a brief and validated scale should make it possible to develop a deeper understanding of the clinical consequences of cerebellar lesions in a wide range of neurological and neuropsychiatric disorders with a link to the cerebellum.