Clinical Review for Healthcare Professionals

Dysarthria is a motor speech disorder characterized by poorly articulated, slurred, and often nasal speech caused by weakness or incoordination of the muscles used in speech production. It can develop abruptly or gradually and is typically evident during conversation. Differentiation from aphasia, a language disorder affecting speech production or comprehension, is crucial for diagnosis and management.

Pathophysiology

Dysarthria results from disruption of the motor control pathways responsible for coordinating the muscles involved in speech production, including those of the lips, tongue, palate, vocal cords, and respiratory system. The integrity of several neural structures and pathways is essential for normal articulation, phonation, resonance, and prosody:

• Upper and Lower Motor Neurons: Damage to the corticobulbar tracts (upper motor neurons) or cranial nerve nuclei and peripheral nerves (lower motor neurons) impairs voluntary muscle control, causing weakness, spasticity, or flaccidity of speech muscles.

• Cerebellum: Lesions disrupt timing, coordination, and precision of muscle movements, leading to ataxic dysarthria characterized by irregular speech rhythm and scanning speech.

• Basal Ganglia: Involved in motor modulation and muscle tone; lesions cause hypokinetic or hyperkinetic dysarthria seen in Parkinson’s disease and other movement disorders, with reduced or excessive involuntary movements affecting speech.

• Neuromuscular Junction and Muscle: Disorders like myasthenia gravis impair neuromuscular transmission, leading to fatigable weakness of speech muscles and nasal voice quality.

Damage to any of these components interrupts the complex integration necessary for smooth, intelligible speech, resulting in the characteristic features of dysarthria such as slurred, slow, labored, or nasal speech.

Classification and clinical features

• Flaccid Dysarthria: Due to lower motor neuron lesions affecting cranial nerves IX, X, or XII, resulting in nasal voice, weak articulation, and dysphagia.

• Spastic Dysarthria: Caused by upper motor neuron lesions producing slow, strained, and harsh speech.

• Ataxic Dysarthria: From cerebellar dysfunction, characterized by irregular speech rhythm and scanning speech.

• Hypokinetic Dysarthria: Common in Parkinson’s disease, producing monotone, reduced loudness, and imprecise articulation.

• Hyperkinetic Dysarthria: Seen in Huntington’s disease, with involuntary movements affecting speech.

Etiology and associated signs

Emergency interventions

• Assess for dysphagia and respiratory muscle weakness: monitor respiratory rate, depth, vital capacity (if possible).

• Maintain airway patency; position patient in Fowler’s position.

• Suction airway as needed; administer oxygen.

• Prepare for possible intubation and mechanical ventilation in progressive respiratory failure.

• Withhold oral fluids if dysphagia is present to prevent aspiration.

• Conduct thorough neurologic exam if no respiratory compromise: assess muscle strength, tone, sensation, reflexes, gait, cerebellar function, visual fields, facial muscles, and consciousness level.

History and physical examination

• Determine onset, progression, and fluctuation of dysarthria.

• Ask about associated swallowing difficulty and respiratory symptoms.

• Review medication, alcohol use, and history of seizures.

• Examine denture fit.

• Differentiate dysarthria from aphasia via speech tests.

Diagnosis

• Clinical evaluation emphasizing speech and neurologic examination.

• Neuroimaging (MRI preferred) for structural brainstem or cerebellar lesions.

• Electromyography (EMG) or nerve conduction studies if neuromuscular disorder suspected.

• Laboratory testing based on suspected etiology (e.g., thiamine levels, toxicology).

Management

• Treat underlying cause (e.g., thiamine for Wernicke’s encephalopathy, antivirals for encephalitis).

• Supportive care including airway management and swallowing precautions.

• Speech therapy consultation for rehabilitation.

• Patient counseling on communication strategies; encourage slow speech and use of gestures.

• Multidisciplinary care involving neurology, speech pathology, and occupational therapy.

Pediatric considerations

• Common causes include brainstem gliomas and cerebral palsy.

• Early diagnosis is challenging due to immature speech.

• Look for associated neurologic deficits.

• Encourage early speech therapy; prognosis is generally better than adults.

Prognosis

• Varies with underlying cause.

• Progressive neurodegenerative diseases tend to worsen.

• Reversible causes (e.g., toxins, infections) may improve with treatment.

• Early intervention improves outcomes.