Dysarthria is a motor speech disorder resulting from neurological injury that impairs the muscles responsible for speech production. This damage interferes with the control over the muscles of the face, tongue, throat, and respiratory system necessary for clear communication. Individuals with dysarthria struggle with the physical execution of speech, often resulting in slurred, slow, or difficult-to-understand speech. The disorder can affect any of the five subsystems of speech: respiration, phonation (voice production), resonance, articulation, and prosody (rhythm and stress).
Understanding the Neurological Basis
The variety of dysarthria types is determined by the specific location of the neurological damage within the nervous system. Neurologists and speech-language pathologists use a standard classification system to link perceptual speech characteristics to the site of the lesion. This framework differentiates the types based on whether the damage affects the central nervous system (CNS), the peripheral nervous system (PNS), or specific control circuits in the brain.
The distinction between Upper Motor Neurons (UMN) and Lower Motor Neurons (LMN) is fundamental to this classification. UMNs originate in the cerebral cortex and brainstem, carrying signals down to the LMNs to orchestrate voluntary movement. LMNs are the final common pathway, carrying the signal directly from the brainstem or spinal cord to the speech muscles.
Damage to UMN pathways often results in spasticity and increased muscle tone because inhibitory control is lost. Conversely, damage to LMNs or peripheral nerves leads to muscle weakness and reduced tone, as the direct signal to the muscle is interrupted. The specific type of dysarthria reflects the disruption to one of these motor pathways or control circuits.
Flaccid and Spastic Dysarthria
Flaccid dysarthria arises from damage to the Lower Motor Neurons (LMNs) or the cranial nerves that innervate the speech muscles. This damage interrupts the neural impulse, resulting in muscle weakness, reduced muscle tone (hypotonia), and diminished reflexes. Conditions like Myasthenia Gravis, brainstem stroke, or cranial nerve injury can cause this dysarthria.
The speech is characterized by auditory features stemming from this muscle weakness. The voice often sounds breathy or whispery because the vocal folds cannot fully adduct. Weakness in the soft palate causes hypernasality, where excessive air escapes through the nose. Speech typically includes imprecise consonants, short phrases, and sometimes audible inspiration.
Spastic dysarthria results from bilateral damage to the Upper Motor Neurons (UMNs). This damage causes a combination of weakness and spasticity, meaning the muscles are both weak and excessively tense (hypertonic). It is often caused by multiple strokes or progressive diseases like Amyotrophic Lateral Sclerosis (ALS), which affects both UMNs and LMNs.
The resulting speech has a strained or strangled vocal quality, reflecting the effort to push air past tense vocal folds. The rate of speech is slow and laborious, with imprecise articulation due to reduced range of motion in the articulators. Prosody is often affected, resulting in a monotone pitch and monoloudness because the tense muscles cannot vary in force or range of movement.
Ataxic and Hypokinetic Dysarthria
Ataxic dysarthria is caused by damage to the cerebellum, which coordinates voluntary movements and controls timing. The cerebellum ensures smooth, accurate muscle activity, so its damage leads to a breakdown in the timing and force of speech movements. The resulting motor characteristic is incoordination, which affects the entire speech mechanism.
The speech is often described as sounding “drunk” or slurred due to irregular articulatory breakdowns. A hallmark feature is “excess and equal stress,” where the normal rhythm is lost and each syllable is given the same emphasis, creating a choppy pattern. Irregular timing and distorted vowels are also common, reflecting the lack of precision in muscle control.
Hypokinetic dysarthria is strongly associated with Parkinson’s Disease and results from damage to the basal ganglia control circuit, specifically the depletion of dopamine. The term “hypokinetic” refers to the reduced range and slowness of movement, including difficulty with movement initiation. This basal ganglia dysfunction leads to rigidity and reduced range of motion in the speech musculature.
The speech profile is characterized by a reduction in vocal loudness, often described as a soft or quiet voice (hypophonia). The voice is monotone and lacks natural inflection, reflecting the rigidity and reduced prosodic range. A distinctive feature is “rushes of speech,” where the rate rapidly accelerates, leading to mumbling and severely imprecise articulation.
Hyperkinetic and Mixed Dysarthria
Hyperkinetic dysarthria results from damage to the basal ganglia control circuit, but this damage leads to abnormal, involuntary movements, unlike hypokinetic dysarthria. These involuntary movements—such as tremors, tics, or chorea—unpredictably interrupt the flow of speech. The specific speech characteristics depend on the type of underlying movement disorder, such as the chorea seen in Huntington’s disease.
Speech is marked by prosodic abnormalities, including sudden, irregular pitch and loudness variations, and intermittent voice stoppages. Irregular articulatory breakdowns occur because involuntary movements of the tongue, jaw, or larynx interfere with the intended speech movements. This gives the speech a jerky, unpredictable quality.
Mixed dysarthria is the most common presentation in clinical practice, occurring when multiple areas of the nervous system are damaged. This type combines the perceptual features of two or more “pure” dysarthria types. It results from diffuse or multifocal neurological diseases like Traumatic Brain Injury (TBI), Multiple Sclerosis (MS), or Amyotrophic Lateral Sclerosis (ALS).
For example, ALS frequently causes a combination of flaccid dysarthria (from LMN damage) and spastic dysarthria (from UMN damage). The resulting speech includes the strained-strangled voice of spastic dysarthria alongside the hypernasality and breathiness of flaccid dysarthria. The overall features reflect a complex blend of weakness, slowness, and incoordination.