Where is the lesion in a patient with dysarthria (difficulty speaking)?

From the Guidelines

Dysarthria is caused by lesions in the central or peripheral nervous system that affect the muscles involved in speech production, with possible locations including the cerebral cortex, cerebellum, basal ganglia, brainstem, cranial nerves, or neuromuscular junction. The lesion can be located in several areas, and the specific location determines the type of dysarthria. According to 1, dysarthria can affect any of the subsystems underlying speech production, including the respiratory, laryngeal, velopharyngeal, and oral-articulatory subsystems. The clinical presentation, including specific speech characteristics, helps localize the lesion.

Possible Locations of the Lesion

• Cerebral cortex (particularly the motor cortex)
• Cerebellum
• Basal ganglia
• Brainstem
• Cranial nerves (especially V, VII, IX, X, and XII)
• Neuromuscular junction

Types of Dysarthria

• Flaccid dysarthria: results from lower motor neuron damage to cranial nerves
• Spastic dysarthria: results from bilateral upper motor neuron damage
• Ataxic dysarthria: results from cerebellar damage
• Hypokinetic dysarthria: results from basal ganglia involvement (particularly in Parkinson's disease)
• Hyperkinetic dysarthria: results from basal ganglia disorders causing involuntary movements
• Mixed dysarthria: results from multiple lesion sites As noted in 1, careful neurological examination focusing on speech patterns, cranial nerve function, and motor control is essential for accurate localization and appropriate management of the underlying condition. A certified speech and language pathologist normally performs the evaluation and treatment of communication disorders, including dysarthria.

From the Research

Lesion Location in Dysarthria

The location of the lesion in a patient with dysarthria can vary depending on the type of dysarthria and the underlying neuropathology.

• Dysarthria can be classified into six major types: flaccid, spastic, ataxic, hyperkinetic, hypokinetic, and mixed dysarthria, each associated with different lesion locations 2.
• Lesions in the left hemisphere, particularly in the lower motor cortex, striatocapsular region, and base of the pons, can cause dysarthria with predominant articulatory abnormalities 3.
• Cerebellar lesions, specifically in the rostral paravermal region of the anterior lobe, can also lead to dysarthria, characterized by articulatory movements of the tongue and orofacial muscles 4.
• Subcortical lesions, including those in the basal ganglia and thalamus, can impact speech production, with the left thalamus and putamen correlated with concept preparation and word retrieval, and the globus pallidus and caudate nucleus affecting larynx and tongue movements 5.

Lesion Topography

Lesion topography plays a crucial role in determining the type and severity of dysarthria.

• Extracerebellar infarctions, particularly those in the left hemisphere, can cause more severe dysarthria 3.
• Cerebellar lesions, especially those in the superior cerebellar artery territory, can lead to dysarthria with distinct speech characteristics 4.
• Subcortical lesions, including those in the basal ganglia and thalamus, can impact speech production, with lateralization and hierarchical organization of each nucleus contributing to their roles in speech functions 5.

Clinical Implications

Understanding the lesion location and topography in dysarthria can have significant clinical implications.

• Early assessment and identification of dysarthria type and severity can facilitate differential diagnosis and optimize healthcare service distribution 6.
• Objective measurements of acoustic parameters and speech characteristics can help monitor progress in the acute phase post-stroke 6.
• A nuanced understanding of the subcortical neuromechanisms underlying dysarthria can contribute to the development of personalized treatment plans and multimodal assessment indicators 5.