Neurologic and Neurodegenerative Diseases of the Larynx by Philip A. Weissbrod & David O. Francis

Author:Philip A. Weissbrod & David O. Francis
Language: eng
Format: epub
ISBN: 9783030288525
Publisher: Springer International Publishing

Dysarthria

Dysarthria is the dysfunction in initiation, coordination, and control of articulatory structures involved in speech. The pathway for speech articulation was initially thought to be the corticobulbar tracts; however, extrapyramidal inputs from the cerebellum and basal ganglia have been found to play significant roles in articulation [35]. Lacunar infarcts to the deep cortex and brainstem are the most common causes of post-stroke dysarthria, with roughly equivalent incidence of 46% and 54%, respectively [36]. Supratentorial lesions in the distribution of the left MCA lead to upper motor neuron damage causing increased tone in the muscles of speech leading to spastic dysarthria. Weakness of the face or tongue, hemiparesis, hyperreflexia, spasticity, hemianopia, and the Babinski sign typically accompany the dysarthria symptoms. Infratentorial infarcts of the lower motor neurons in the pontine base lead to flaccid dysarthria. Basilar artery and PICA infarctions may involve the nucleus ambiguus as well as the facial and hypoglossal nuclei leading to coincidence of face, tongue, or palatal weakness, dysphonia, and dysphagia with dysarthria.

The extrapyramidal system controls automatic movements by modulating the lower motor neurons of the pyramidal tract with multisynaptic and indirect connections. Due to the complex nature of the connections between these centers, there is controversy regarding the precise regions involved in post-stroke dysarthria [36–38]. The basal ganglia receive cortical input to the caudate and putamen which in turn project to the globus pallidus which sends signals to the motor thalamus in order to regulate the motor cortex via either excitatory or inhibitory signals. Lesions of the basal ganglia arise from obstruction of the deep penetrating arteries of the MCA and ACA. Hyper- or hypokinetic dysarthria can result from these strokes due to impaired neuroregulation of cortical motor signals. Hyperkinetic dysarthria is caused by irregular, inaccurate, and spastic movement in the form of chorea or dystonia. Hypokinetic dysarthria is marked by reduced amplitude and range of movements, which can be seen in Parkinson disease. Lesions in the cerebellum cause inaccurate direction and rhythm of movement, slowed movement, and flaccidity. The resulting ataxic dysarthria is characterized by poor coordination of speech and respiration as well as a “scanning” quality due to unnatural separation of syllables. Dysdiadokokinesia, dysmetria, nystagmus, and truncal ataxia are commonly seen in these patients due to collateral damage to the cerebellum.

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