K K Jain MD (

Dr. Jain is a consultant in neurology and has no relevant financial relationships to disclose.

Originally released April 3, 2007; last updated March 27, 2020; expires March 27, 2023

This article includes discussion of dysarthria, progressive dysarthria, nonprogressive dysarthria, spastic dysarthria, and flaccid dysarthria. The foregoing terms may include synonyms, similar disorders, variations in usage, and abbreviations.


This article discusses the evaluation of dysarthria as a symptom of neurologic disorders. It can be due to lesions at several levels from the cortex down to cranial nerves. A well-known type is ataxic dysarthria due to cerebellar lesions. Several diseases can manifest with dysarthria. Diagnostic work-up and differential diagnosis depend on clinical suspicion of the cause. Prognosis depends on the underlying pathology. Management is directed at the cause if treatable. The mainstay of management is speech therapy, and variable results have been reported.

Key points


• Dysarthria is a manifestation of several disorders, both systemic and neurologic, that affect coordination of speech.


• For management purposes, it is important to differentiate dysarthria from other disorders of speech.


• Prognosis of dysarthria depends on the nature of the lesion; prognosis is poor in neurodegenerative disorders and better in stroke.


• Usefulness of speech therapy in improving articulation varies according to the nature of lesion causing dysarthria.

Historical note and terminology

Dysarthria is defined as difficulty in articulation of words due to neurologic disturbances of function of orofacial muscles, tongue, lips, and throat. Total inability to articulate is termed anarthria. The broad term "disorders of articulation" includes many other motor disorders of speech such as stuttering (also called stammering), which is a disturbance of verbal fluency. Dyslalia is disturbance of speech due to structural damage to the apparatus for articulation without structural neurologic deficit. Most of the investigations of speech in early development of neurology were focused on aphasia but dysarthria was noted as a manifestation of several neurologic disorders. Charcot described the triad of scanning speech, ataxia, and nystagmus in multiple sclerosis (Charcot 1877). Initially, neurologic localization of dysarthria was based on correlation with pathological lesions noted at autopsy. Penfield was the first to map the cerebral area for vocalization, on the precentral gyrus between the responses of hand movement and throat movement, by electrical stimulation of the cortex in conscious persons (Penfield 1938).

Abnormalities of domains of speech relevant to dysarthria are: (1) articulation may be slow and consonants are imprecise; (2) instability of pitch and loudness of voice; (3) decreased time for phonation expiratory pressure; and (4) longer and frequent pauses with deficient control of loudness. The modern classification of the dysarthrias still rests largely on Darley's classical study of 1969 (Darley et al 1969). Brain imaging studies have added some information about localization of lesions. For practical purposes, the following 6 types of dysarthria are still referred to in differential diagnosis and planning of treatment:


(1) Flaccid: lower motor neuron, eg, cranial nerve involvement
(2) Spastic: upper motor neuron, eg, stroke
(3) Spastic-flaccid: both upper and lower motor neurons, eg, multiple sclerosis
(4) Ataxic: cerebellum or its outflow pathways, eg, cerebellar lesions
(5) Hypokinetic: basal ganglia, especially substantial nigra, eg, Parkinson disease
(6) Hyperkinetic: basal ganglia, especially putamen, caudate, or both, eg, Huntington disease.

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