Associated with damage to the cerebellar control circuit,

causing in-coordination and poor muscle tone.

Produces slowness and inaccuracy in force, range, timing, & direction of speech movement.

Halting, imprecise, jerky, poorly coordinated, and lacking in speed and fluidity.

Affect articulation and prosody.

Sometimes perceived as slurred speech with a "drunken quality".

Produced by bilateral damage to the direct and indirect activation pathways of the Central Nervous System (CNS), often associaled with upper motor neuron disease.

Characteristics reflect the combined effects of weakness and spasticity (excessive muscle tone) in a way that slows movement and reduces its range and force.

Predominant causes:  Degenerative (e.g., ALS), vascular, and traumatic disorders.

Drooling is common, likely due to decreased frequency of swallowing.

Slowed jaw, lip, and facial movement.

The face may be held in a somewhat fixed, subtle smiling or pouting posture.

Display of pseudobulbar affect (lability of affect) is common.

Patient may cry or laugh in a stereotypic manner for no apparent reason.  May fluctuate between laughing and crying or have difficulty inhibiting laughter or crying once they begin.

How easily the response is triggered if often related to the emotional loading of the interaction.

Conversational speech, reading, & speech AMR are the most useful tasks for eliciting salient chracteristics.

Associated with impaired movement patterns, rather than weakness of individual muscles. 

Deficits seen at all speech valves and for all components of speech, though not always equally.  Intelligibility is often affected due to the involvement of multiple speech valves.

Chief disturbances are slowness and reduced range of individual and repetitive movements, reduced force of movement, and excessive or biased muscle tone or spasticity.

Strained-harsh voice quality, slow speech rate, and slow/regular AMRs are the most distinctive clues to the presence of spastic dysarthria

Produced by injury of malfunction of one or more of the cranial or spinal nerves. Reflect problems in the nuclei, neurons, or neuromuscular junctions that make up the motor units of the fnal common pathway.

May manifest in any or all respiratory, phonatory, or articulatory speech components.

Due to muscle weakness and reduced muscle tone, affects speed, range, and accuracy of speech.

Involvement can invovle single or mutiple muscle groups.

Can be caused by any process that damages the motor unit.

Trauma is the most common cause of peripheral or cranial nerve lesions when a single nerve is injured.

Lesions lead to weakness of jaw muscles & when bilateral, can have significant effects on articulation.

Also affect sensation from the jaw, face, lip, and tongue.

May affect speech by way of articulatory precision.

Lesions can lead to facial weakness,

Unilateral associated with mild articulatory distortions.

Bilateral may lead to significant distortion of all consonants and vowels requiring facial movement.

Lesions can lead to weakness of velopharyngeal and laryngeal muscles depending on which branch is affected.

• pharyngeal lesions lead to resonatory incompetence w/ hypernasality, nasal emission, & weakening of pressure consonant sounds.
• laryngeal branches can lead to dysphonias w/ perceptual attributes consistent w/ weakness & hypotonia of laryngeal muscles

Lesions can cause tongue weakness.

Reflected in imprecision of lingual articulation.

Degree of severity dependent on whether the lesion is uni- or bilateral.

Lesions can reduce respiratory support for speech.

Weakness can lead to reduced loudness and pitch variability and reduced phrase per breath group.